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  • Rats  (534)
  • American Association for the Advancement of Science (AAAS)  (534)
  • American Institute of Physics (AIP)
  • 2005-2009  (208)
  • 1995-1999  (326)
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  • 1
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    DNA binding site sequence directs glucocorticoid receptor structure and activity (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-18
    Description: Genes are not simply turned on or off, but instead their expression is fine-tuned to meet the needs of a cell. How genes are modulated so precisely is not well understood. The glucocorticoid receptor (GR) regulates target genes by associating with specific DNA binding sites, the sequences of which differ between genes. Traditionally, these binding sites have been viewed only as docking sites. Using structural, biochemical, and cell-based assays, we show that GR binding sequences, differing by as little as a single base pair, differentially affect GR conformation and regulatory activity. We therefore propose that DNA is a sequence-specific allosteric ligand of GR that tailors the activity of the receptor toward specific target genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777810/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777810/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meijsing, Sebastiaan H -- Pufall, Miles A -- So, Alex Y -- Bates, Darren L -- Chen, Lin -- Yamamoto, Keith R -- GM08537/GM/NIGMS NIH HHS/ -- R01 CA020535/CA/NCI NIH HHS/ -- R01 CA020535-31/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):407-10. doi: 10.1126/science.1164265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19372434" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Binding Sites ; Cell Line, Tumor ; Crystallography, X-Ray ; DNA/*chemistry/*metabolism ; Humans ; Ligands ; Models, Molecular ; Mutation ; Protein Conformation ; Protein Isoforms/chemistry/metabolism ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rats ; Receptors, Glucocorticoid/chemistry/genetics/*metabolism ; Transcriptional Activation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Regulation of neuronal survival factor MEF2D by chaperone-mediated autophagy (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-03
    Description: Chaperone-mediated autophagy controls the degradation of selective cytosolic proteins and may protect neurons against degeneration. In a neuronal cell line, we found that chaperone-mediated autophagy regulated the activity of myocyte enhancer factor 2D (MEF2D), a transcription factor required for neuronal survival. MEF2D was observed to continuously shuttle to the cytoplasm, interact with the chaperone Hsc70, and undergo degradation. Inhibition of chaperone-mediated autophagy caused accumulation of inactive MEF2D in the cytoplasm. MEF2D levels were increased in the brains of alpha-synuclein transgenic mice and patients with Parkinson's disease. Wild-type alpha-synuclein and a Parkinson's disease-associated mutant disrupted the MEF2D-Hsc70 binding and led to neuronal death. Thus, chaperone-mediated autophagy modulates the neuronal survival machinery, and dysregulation of this pathway is associated with Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Qian -- She, Hua -- Gearing, Marla -- Colla, Emanuela -- Lee, Michael -- Shacka, John J -- Mao, Zixu -- AG023695/AG/NIA NIH HHS/ -- NS038065/NS/NINDS NIH HHS/ -- NS048254/NS/NINDS NIH HHS/ -- NS055077/NS/NINDS NIH HHS/ -- NS47466/NS/NINDS NIH HHS/ -- NS57098/NS/NINDS NIH HHS/ -- P30 NS055077/NS/NINDS NIH HHS/ -- P30 NS055077-01A2/NS/NINDS NIH HHS/ -- P50 AG025688/AG/NIA NIH HHS/ -- P50 AG025688-03/AG/NIA NIH HHS/ -- R01 AG023695/AG/NIA NIH HHS/ -- R01 AG023695-02/AG/NIA NIH HHS/ -- R01 AG023695-03/AG/NIA NIH HHS/ -- R01 AG023695-04/AG/NIA NIH HHS/ -- R01 AG023695-05/AG/NIA NIH HHS/ -- R01 NS048254/NS/NINDS NIH HHS/ -- R01 NS048254-02/NS/NINDS NIH HHS/ -- R01 NS048254-03/NS/NINDS NIH HHS/ -- R01 NS048254-04/NS/NINDS NIH HHS/ -- R01 NS048254-05/NS/NINDS NIH HHS/ -- R01 NS048254-06/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Jan 2;323(5910):124-7. doi: 10.1126/science.1166088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119233" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Ammonium Chloride/pharmacology ; Animals ; *Autophagy ; Brain/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Cell Survival ; Cytoplasm/metabolism ; DNA/metabolism ; HSC70 Heat-Shock Proteins/metabolism ; Lysosomal-Associated Membrane Protein 2/metabolism ; Lysosomes/metabolism ; MADS Domain Proteins/*metabolism ; MEF2 Transcription Factors ; Mice ; Mice, Transgenic ; Molecular Chaperones/*metabolism ; Myogenic Regulatory Factors/chemistry/*metabolism ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Protein Binding ; Protein Transport ; Rats ; Rats, Long-Evans ; alpha-Synuclein/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-02-14
    Description: The sigma-1 receptor is widely distributed in the central nervous system and periphery. Originally mischaracterized as an opioid receptor, the sigma-1 receptor binds a vast number of synthetic compounds but does not bind opioid peptides; it is currently considered an orphan receptor. The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947205/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fontanilla, Dominique -- Johannessen, Molly -- Hajipour, Abdol R -- Cozzi, Nicholas V -- Jackson, Meyer B -- Ruoho, Arnold E -- F31 DA022932/DA/NIDA NIH HHS/ -- NS30016/NS/NINDS NIH HHS/ -- R01 MH065503/MH/NIMH NIH HHS/ -- R01 MH065503-01A1/MH/NIMH NIH HHS/ -- R01 NS030016/NS/NINDS NIH HHS/ -- R01 NS030016-08/NS/NINDS NIH HHS/ -- R01 NS030016-09/NS/NINDS NIH HHS/ -- T32 GM08688/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2009 Feb 13;323(5916):934-7. doi: 10.1126/science.1166127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; COS Cells ; Cell Line ; Cells, Cultured ; Cercopithecus aethiops ; Guinea Pigs ; Hallucinogens/*metabolism ; Ligands ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/metabolism ; N,N-Dimethyltryptamine/*metabolism ; Rats ; Receptors, sigma/agonists/antagonists & inhibitors/*metabolism ; Tryptamines/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Extinction-reconsolidation boundaries: key to persistent attenuation of fear memories (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-04-04
    Description: Dysregulation of the fear system is at the core of many psychiatric disorders. Much progress has been made in uncovering the neural basis of fear learning through studies in which associative emotional memories are formed by pairing an initially neutral stimulus (conditioned stimulus, CS; e.g., a tone) to an unconditioned stimulus (US; e.g., a shock). Despite recent advances, the question of how to persistently weaken aversive CS-US associations, or dampen traumatic memories in pathological cases, remains a major dilemma. Two paradigms (blockade of reconsolidation and extinction) have been used in the laboratory to reduce acquired fear. Unfortunately, their clinical efficacy is limited: Reconsolidation blockade typically requires potentially toxic drugs, and extinction is not permanent. Here, we describe a behavioral design in which a fear memory in rats is destabilized and reinterpreted as safe by presenting an isolated retrieval trial before an extinction session. This procedure permanently attenuates the fear memory without the use of drugs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625935/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3625935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monfils, Marie-H -- Cowansage, Kiriana K -- Klann, Eric -- LeDoux, Joseph E -- F31 MH083472/MH/NIMH NIH HHS/ -- F31 MH083472-01A1/MH/NIMH NIH HHS/ -- F31MH083472/MH/NIMH NIH HHS/ -- K05 MH067048/MH/NIMH NIH HHS/ -- NS034007/NS/NINDS NIH HHS/ -- NS047384/NS/NINDS NIH HHS/ -- P50 MH058911/MH/NIMH NIH HHS/ -- R01 MH046516/MH/NIMH NIH HHS/ -- R37 MH038774/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 May 15;324(5929):951-5. doi: 10.1126/science.1167975. Epub 2009 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neural Science, New York University, New York, NY 10003, USA. monfils@mail.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19342552" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/physiology ; Animals ; Conditioning, Classical ; Extinction, Psychological/*physiology ; *Fear ; Male ; Memory/*physiology ; Mental Recall/*physiology ; Phosphorylation ; Rats ; Receptors, AMPA/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    KLF family members regulate intrinsic axon regeneration ability (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: Neurons in the central nervous system (CNS) lose their ability to regenerate early in development, but the underlying mechanisms are unknown. By screening genes developmentally regulated in retinal ganglion cells (RGCs), we identified Kruppel-like factor-4 (KLF4) as a transcriptional repressor of axon growth in RGCs and other CNS neurons. RGCs lacking KLF4 showed increased axon growth both in vitro and after optic nerve injury in vivo. Related KLF family members suppressed or enhanced axon growth to differing extents, and several growth-suppressive KLFs were up-regulated postnatally, whereas growth-enhancing KLFs were down-regulated. Thus, coordinated activities of different KLFs regulate the regenerative capacity of CNS neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882032/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2882032/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moore, Darcie L -- Blackmore, Murray G -- Hu, Ying -- Kaestner, Klaus H -- Bixby, John L -- Lemmon, Vance P -- Goldberg, Jeffrey L -- P30 EY014801/EY/NEI NIH HHS/ -- R01 NS059866/NS/NINDS NIH HHS/ -- R01 NS059866-01A2/NS/NINDS NIH HHS/ -- R01 NS061348/NS/NINDS NIH HHS/ -- R01 NS061348-01A2/NS/NINDS NIH HHS/ -- R01 NS061348-02/NS/NINDS NIH HHS/ -- R01 NS061348-03/NS/NINDS NIH HHS/ -- R01 NS061348-04/NS/NINDS NIH HHS/ -- R03 EY016790/EY/NEI NIH HHS/ -- R03 EY016790-01/EY/NEI NIH HHS/ -- R03 EY016790-02/EY/NEI NIH HHS/ -- R03 EY016790-03/EY/NEI NIH HHS/ -- T32 NS007459/NS/NINDS NIH HHS/ -- T32 NS07492/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):298-301. doi: 10.1126/science.1175737.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815778" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Count ; Cell Survival ; Cells, Cultured ; Down-Regulation ; Gene Knockout Techniques ; Growth Cones/physiology ; Hippocampus/cytology/physiology ; Kruppel-Like Transcription Factors/genetics/*physiology ; Mice ; Nerve Crush ; Nerve Regeneration ; Neurites/physiology ; Neurons/*physiology ; Optic Nerve Injuries/physiopathology ; Rats ; Retinal Ganglion Cells/cytology/*physiology ; Transcription, Genetic ; Transfection ; Up-Regulation
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Burst spiking of a single cortical neuron modifies global brain state (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-02
    Description: Different global patterns of brain activity are associated with distinct arousal and behavioral states of an animal, but how the brain rapidly switches between different states remains unclear. We here report that repetitive high-frequency burst spiking of a single rat cortical neuron could trigger a switch between the cortical states resembling slow-wave and rapid-eye-movement sleep. This is reflected in the switching of the membrane potential of the stimulated neuron from slow UP/DOWN oscillations to a persistent-UP state or vice versa, with concurrent changes in the temporal pattern of cortical local field potential (LFP) recorded several millimeters away. These results point to the power of single cortical neurons in modulating the behavioral state of an animal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913066/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Cheng-Yu T -- Poo, Mu-Ming -- Dan, Yang -- R01 EY018861/EY/NEI NIH HHS/ -- R01 EY018861-01/EY/NEI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2009 May 1;324(5927):643-6. doi: 10.1126/science.1169957.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Institute of Neuroscience, University of California, Berkeley, CA 94720, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19407203" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Electroencephalography ; Membrane Potentials ; Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Long-Evans ; Sleep Stages ; Sleep, REM ; Somatosensory Cortex/cytology/*physiology ; Visual Cortex/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Knockout rats via embryo microinjection of zinc-finger nucleases (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-25
    Description: The toolbox of rat genetics currently lacks the ability to introduce site-directed, heritable mutations into the genome to create knockout animals. By using engineered zinc-finger nucleases (ZFNs) designed to target an integrated reporter and two endogenous rat genes, Immunoglobulin M (IgM) and Rab38, we demonstrate that a single injection of DNA or messenger RNA encoding ZFNs into the one-cell rat embryo leads to a high frequency of animals carrying 25 to 100% disruption at the target locus. These mutations are faithfully and efficiently transmitted through the germline. Our data demonstrate the feasibility of targeted gene disruption in multiple rat strains within 4 months time, paving the way to a humanized monoclonal antibody platform and additional human disease models.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831805/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geurts, Aron M -- Cost, Gregory J -- Freyvert, Yevgeniy -- Zeitler, Bryan -- Miller, Jeffrey C -- Choi, Vivian M -- Jenkins, Shirin S -- Wood, Adam -- Cui, Xiaoxia -- Meng, Xiangdong -- Vincent, Anna -- Lam, Stephen -- Michalkiewicz, Mieczyslaw -- Schilling, Rebecca -- Foeckler, Jamie -- Kalloway, Shawn -- Weiler, Hartmut -- Menoret, Severine -- Anegon, Ignacio -- Davis, Gregory D -- Zhang, Lei -- Rebar, Edward J -- Gregory, Philip D -- Urnov, Fyodor D -- Jacob, Howard J -- Buelow, Roland -- 5P01HL082798-03/HL/NHLBI NIH HHS/ -- 5U01HL066579-08/HL/NHLBI NIH HHS/ -- P01 HL082798/HL/NHLBI NIH HHS/ -- P01 HL082798-03/HL/NHLBI NIH HHS/ -- U01 HL066579/HL/NHLBI NIH HHS/ -- U01 HL066579-08/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):433. doi: 10.1126/science.1172447.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human and Molecular Genetics Center, Medical College of Wisconsin, Milwaukee, WI 52336, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19628861" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Dna ; Embryo, Mammalian ; Endodeoxyribonucleases/genetics/*metabolism ; Feasibility Studies ; Female ; *Gene Knockout Techniques ; Green Fluorescent Proteins ; Immunoglobulin M/*genetics ; Male ; *Microinjections ; Molecular Sequence Data ; Mutagenesis, Site-Directed ; RNA, Messenger ; Rats ; *Zinc Fingers/genetics ; rab GTP-Binding Proteins/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Identification of splenic reservoir monocytes and their deployment to inflammatory sites (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-01
    Description: A current paradigm states that monocytes circulate freely and patrol blood vessels but differentiate irreversibly into dendritic cells (DCs) or macrophages upon tissue entry. Here we show that bona fide undifferentiated monocytes reside in the spleen and outnumber their equivalents in circulation. The reservoir monocytes assemble in clusters in the cords of the subcapsular red pulp and are distinct from macrophages and DCs. In response to ischemic myocardial injury, splenic monocytes increase their motility, exit the spleen en masse, accumulate in injured tissue, and participate in wound healing. These observations uncover a role for the spleen as a site for storage and rapid deployment of monocytes and identify splenic monocytes as a resource that the body exploits to regulate inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803111/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2803111/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Swirski, Filip K -- Nahrendorf, Matthias -- Etzrodt, Martin -- Wildgruber, Moritz -- Cortez-Retamozo, Virna -- Panizzi, Peter -- Figueiredo, Jose-Luiz -- Kohler, Rainer H -- Chudnovskiy, Aleksey -- Waterman, Peter -- Aikawa, Elena -- Mempel, Thorsten R -- Libby, Peter -- Weissleder, Ralph -- Pittet, Mikael J -- 1R01HL095612/HL/NHLBI NIH HHS/ -- P01 A154904/PHS HHS/ -- P01 AI054904/AI/NIAID NIH HHS/ -- P01 AI054904-010001/AI/NIAID NIH HHS/ -- P50 CA086355/CA/NCI NIH HHS/ -- P50 CA086355-07/CA/NCI NIH HHS/ -- P50 CA86355/CA/NCI NIH HHS/ -- R00 HL094533/HL/NHLBI NIH HHS/ -- R01 HL095629/HL/NHLBI NIH HHS/ -- R01 HL096576/HL/NHLBI NIH HHS/ -- R24 CA69246/CA/NCI NIH HHS/ -- U01 HL080731/HL/NHLBI NIH HHS/ -- U01 HL080731-05/HL/NHLBI NIH HHS/ -- U54 CA126515/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):612-6. doi: 10.1126/science.1175202.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. fswirski@mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644120" target="_blank"〉PubMed〈/a〉
    Keywords: Angiotensin II/blood/pharmacology ; Animals ; Antigens, Ly/metabolism ; Bone Marrow Cells/physiology ; Cell Differentiation ; Cell Movement ; Cell Size ; Female ; Inflammation/*pathology ; Mice ; Mice, Inbred C57BL ; Monocytes/cytology/*physiology ; Myocardial Infarction/immunology/*pathology/*physiopathology ; Myocardium/*immunology/*pathology ; Rats ; Rats, Wistar ; Receptors, Angiotensin/metabolism ; Spleen/cytology/*immunology ; Splenectomy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    The structure of rat liver vault at 3.5 angstrom resolution (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-01-20
    Description: Vaults are among the largest cytoplasmic ribonucleoprotein particles and are found in numerous eukaryotic species. Roles in multidrug resistance and innate immunity have been suggested, but the cellular function remains unclear. We have determined the x-ray structure of rat liver vault at 3.5 angstrom resolution and show that the cage structure consists of a dimer of half-vaults, with each half-vault comprising 39 identical major vault protein (MVP) chains. Each MVP monomer folds into 12 domains: nine structural repeat domains, a shoulder domain, a cap-helix domain, and a cap-ring domain. Interactions between the 42-turn-long cap-helix domains are key to stabilizing the particle. The shoulder domain is structurally similar to a core domain of stomatin, a lipid-raft component in erythrocytes and epithelial cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, Hideaki -- Kato, Koji -- Yamashita, Eiki -- Sumizawa, Tomoyuki -- Zhou, Yong -- Yao, Min -- Iwasaki, Kenji -- Yoshimura, Masato -- Tsukihara, Tomitake -- New York, N.Y. -- Science. 2009 Jan 16;323(5912):384-8. doi: 10.1126/science.1164975.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Protein Research, Osaka University, 3-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19150846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Crystallization ; Crystallography, X-Ray ; Dimerization ; Liver/*chemistry ; Models, Molecular ; Protein Conformation ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Rats ; Vault Ribonucleoprotein Particles/*chemistry
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  • 10
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    Dopamine controls persistence of long-term memory storage (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-08-22
    Description: The paradigmatic feature of long-term memory (LTM) is its persistence. However, little is known about the mechanisms that make some LTMs last longer than others. In rats, a long-lasting fear LTM vanished rapidly when the D1 dopamine receptor antagonist SCH23390 was injected into the dorsal hippocampus 12 hours, but not immediately or 9 hours, after the fearful experience. Conversely, intrahippocampal application of the D1 agonist SK38393 at the same critical post-training time converted a rapidly decaying fear LTM into a persistent one. This effect was mediated by brain-derived neurotrophic factor and regulated by the ventral tegmental area (VTA). Thus, the persistence of LTM depends on activation of VTA/hippocampus dopaminergic connections and can be specifically modulated by manipulating this system at definite post-learning time points.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rossato, Janine I -- Bevilaqua, Lia R M -- Izquierdo, Ivan -- Medina, Jorge H -- Cammarota, Martin -- New York, N.Y. -- Science. 2009 Aug 21;325(5943):1017-20. doi: 10.1126/science.1172545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro de Memoria, Instituto do Cerebro, Pontificia Universidade Catolica do Rio Grande do Sul, Porto Alegre, Brazil.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19696353" target="_blank"〉PubMed〈/a〉
    Keywords: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Animals ; Benzazepines/pharmacology ; Brain-Derived Neurotrophic Factor/metabolism ; Dopamine/*physiology ; Dopamine Agonists/pharmacology ; Dopamine Antagonists/pharmacology ; Fear ; Hippocampus/drug effects/*physiology ; Male ; Memory/drug effects/*physiology ; Phosphorylation ; Rats ; Rats, Wistar ; Receptors, Dopamine D1/agonists/antagonists & inhibitors/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Time Factors ; Tyrosine 3-Monooxygenase ; Ventral Tegmental Area/*physiology
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  • 11
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    Input-specific spine entry of soma-derived Vesl-1S protein conforms to synaptic tagging (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-05-16
    Description: Late-phase synaptic plasticity depends on the synthesis of new proteins that must function only in the activated synapses. The synaptic tag hypothesis requires input-specific functioning of these proteins after undirected transport. Confirmation of this hypothesis requires specification of a biochemical tagging activity and an example protein that behaves as the hypothesis predicts. We found that in rat neurons, soma-derived Vesl-1S (Homer-1a) protein, a late-phase plasticity-related synaptic protein, prevailed in every dendrite and did not enter spines. N-methyl-d-aspartate receptor activation triggered input-specific spine entry of Vesl-1S proteins, which met many criteria for synaptic tagging. These results suggest that Vesl-1S supports the hypothesis and that the activity-dependent regulation of spine entry functions as a synaptic tag.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Daisuke -- Ozawa, Fumiko -- Inokuchi, Kaoru -- New York, N.Y. -- Science. 2009 May 15;324(5929):904-9. doi: 10.1126/science.1171498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mitsubishi Kagaku Institute of Life Sciences (MITILS), 11 Minamiooya, Machida, Tokyo 194-8511, Japan. dada@mitils.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19443779" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Carrier Proteins/genetics/*metabolism ; Cells, Cultured ; Dendrites/*metabolism ; Dendritic Spines/*metabolism/ultrastructure ; Hippocampus/cytology/metabolism ; Mice ; *Neuronal Plasticity ; Plasmids ; Protein Transport ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*metabolism ; Synaptic Transmission ; Transfection
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Fast synaptic subcortical control of hippocampal circuits (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-10-17
    Description: Cortical information processing is under state-dependent control of subcortical neuromodulatory systems. Although this modulatory effect is thought to be mediated mainly by slow nonsynaptic metabotropic receptors, other mechanisms, such as direct synaptic transmission, are possible. Yet, it is currently unknown if any such form of subcortical control exists. Here, we present direct evidence of a strong, spatiotemporally precise excitatory input from an ascending neuromodulatory center. Selective stimulation of serotonergic median raphe neurons produced a rapid activation of hippocampal interneurons. At the network level, this subcortical drive was manifested as a pattern of effective disynaptic GABAergic inhibition that spread throughout the circuit. This form of subcortical network regulation should be incorporated into current concepts of normal and pathological cortical function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varga, Viktor -- Losonczy, Attila -- Zemelman, Boris V -- Borhegyi, Zsolt -- Nyiri, Gabor -- Domonkos, Andor -- Hangya, Balazs -- Holderith, Noemi -- Magee, Jeffrey C -- Freund, Tamas F -- HHMI55005608/Howard Hughes Medical Institute/ -- MH-54671/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):449-53. doi: 10.1126/science.1178307.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Medicine, Budapest 1083, Hungary. vargav@koki.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Glutamic Acid/physiology ; Hippocampus/cytology/*physiology ; Inhibitory Postsynaptic Potentials ; Interneurons/*physiology ; Mice ; Neural Inhibition/physiology ; Neural Pathways/physiology ; Neurons, Afferent/*physiology ; Patch-Clamp Techniques ; Photic Stimulation ; Raphe Nuclei/cytology/*physiology ; Rats ; Rats, Sprague-Dawley ; Serotonin/*physiology ; Synapses/*physiology ; Synaptic Potentials/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Ventral tegmental area BDNF induces an opiate-dependent-like reward state in naive rats (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-30
    Description: The neural mechanisms underlying the transition from a drug-nondependent to a drug-dependent state remain elusive. Chronic exposure to drugs has been shown to increase brain-derived neurotrophic factor (BDNF) levels in ventral tegmental area (VTA) neurons. BDNF infusions into the VTA potentiate several behavioral effects of drugs, including psychomotor sensitization and cue-induced drug seeking. We found that a single infusion of BDNF into the VTA promotes a shift from a dopamine-independent to a dopamine-dependent opiate reward system, identical to that seen when an opiate-naive rat becomes dependent and withdrawn. This shift involves a switch in the gamma-aminobutyric acid type A (GABAA) receptors of VTA GABAergic neurons, from inhibitory to excitatory signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913611/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2913611/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vargas-Perez, Hector -- Ting-A Kee, Ryan -- Walton, Christine H -- Hansen, D Micah -- Razavi, Rozita -- Clarke, Laura -- Bufalino, Mary Rose -- Allison, David W -- Steffensen, Scott C -- van der Kooy, Derek -- AA13666/AA/NIAAA NIH HHS/ -- R01 AA013666/AA/NIAAA NIH HHS/ -- R01 AA013666-09/AA/NIAAA NIH HHS/ -- R01 AA020919/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1732-4. doi: 10.1126/science.1168501. Epub 2009 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics, University of Toronto, 160 College Street, Toronto, Ontario M5S 3E1, Canada. vargashector@yahoo.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19478142" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Brain-Derived Neurotrophic Factor/administration & ; dosage/genetics/*metabolism/*pharmacology ; Conditioning (Psychology) ; Dopamine/physiology ; Dopamine Antagonists/administration & dosage/pharmacology ; Flupenthixol/administration & dosage/pharmacology ; GABA Agonists/pharmacology ; GABA Antagonists/pharmacology ; Heroin Dependence/metabolism ; Male ; Morphine/administration & dosage ; Muscimol/pharmacology ; Opioid-Related Disorders/*metabolism ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; *Reward ; Signal Transduction ; Substance Withdrawal Syndrome/metabolism ; Ventral Tegmental Area/drug effects/*metabolism
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  • 14
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    Chronic stress causes frontostriatal reorganization and affects decision-making (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-08-01
    Description: The ability to shift between different behavioral strategies is necessary for appropriate decision-making. Here, we show that chronic stress biases decision-making strategies, affecting the ability of stressed animals to perform actions on the basis of their consequences. Using two different operant tasks, we revealed that, in making choices, rats subjected to chronic stress became insensitive to changes in outcome value and resistant to changes in action-outcome contingency. Furthermore, chronic stress caused opposing structural changes in the associative and sensorimotor corticostriatal circuits underlying these different behavioral strategies, with atrophy of medial prefrontal cortex and the associative striatum and hypertrophy of the sensorimotor striatum. These data suggest that the relative advantage of circuits coursing through sensorimotor striatum observed after chronic stress leads to a bias in behavioral strategies toward habit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dias-Ferreira, Eduardo -- Sousa, Joao C -- Melo, Irene -- Morgado, Pedro -- Mesquita, Ana R -- Cerqueira, Joao J -- Costa, Rui M -- Sousa, Nuno -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 31;325(5940):621-5. doi: 10.1126/science.1171203.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, 4710-057 Braga, Portugal.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19644122" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atrophy ; Cell Count ; Choice Behavior ; Chronic Disease ; Corpus Striatum/*pathology ; *Decision Making ; Dendrites/pathology ; Frontal Lobe/*pathology ; Habits ; Hypertrophy ; Neural Pathways/pathology ; Neurons/pathology ; Prefrontal Cortex/pathology ; Rats ; Rats, Long-Evans ; Rats, Wistar ; Reinforcement (Psychology) ; Stress, Psychological/*pathology/*psychology
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  • 15
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    Overexpression of alpha2A-adrenergic receptors contributes to type 2 diabetes (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Several common genetic variations have been associated with type 2 diabetes, but the exact disease mechanisms are still poorly elucidated. Using congenic strains from the diabetic Goto-Kakizaki rat, we identified a 1.4-megabase genomic locus that was linked to impaired insulin granule docking at the plasma membrane and reduced beta cell exocytosis. In this locus, Adra2a, encoding the alpha2A-adrenergic receptor [alpha(2A)AR], was significantly overexpressed. Alpha(2A)AR mediates adrenergic suppression of insulin secretion. Pharmacological receptor antagonism, silencing of receptor expression, or blockade of downstream effectors rescued insulin secretion in congenic islets. Furthermore, we identified a single-nucleotide polymorphism in the human ADRA2A gene for which risk allele carriers exhibited overexpression of alpha(2A)AR, reduced insulin secretion, and increased type 2 diabetes risk. Human pancreatic islets from risk allele carriers exhibited reduced granule docking and secreted less insulin in response to glucose; both effects were counteracted by pharmacological alpha(2A)AR antagonists.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosengren, Anders H -- Jokubka, Ramunas -- Tojjar, Damon -- Granhall, Charlotte -- Hansson, Ola -- Li, Dai-Qing -- Nagaraj, Vini -- Reinbothe, Thomas M -- Tuncel, Jonatan -- Eliasson, Lena -- Groop, Leif -- Rorsman, Patrik -- Salehi, Albert -- Lyssenko, Valeriya -- Luthman, Holger -- Renstrom, Erik -- New York, N.Y. -- Science. 2010 Jan 8;327(5962):217-20. doi: 10.1126/science.1176827. Epub 2009 Nov 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lund University Diabetes Centre, Malmo, SE-20502 Malmo, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965390" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adrenergic alpha-2 Receptor Agonists ; Adrenergic alpha-2 Receptor Antagonists ; Adrenergic alpha-Agonists/pharmacology ; Adrenergic alpha-Antagonists/pharmacology ; Adult ; Aged ; Animals ; Animals, Congenic ; Blood Glucose/metabolism ; Cell Membrane/metabolism ; Cyclic AMP/metabolism ; Diabetes Mellitus, Type 2/*genetics/metabolism ; Exocytosis ; Genetic Association Studies ; Genetic Predisposition to Disease ; Humans ; Insulin/blood/*secretion ; Insulin-Secreting Cells/*secretion ; Middle Aged ; Polymorphism, Single Nucleotide ; RNA Interference ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, alpha-2/*genetics/*metabolism ; Risk Factors ; Secretory Vesicles/metabolism ; Up-Regulation ; Young Adult
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  • 16
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    Induction of synaptic long-term potentiation after opioid withdrawal (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-07-11
    Description: mu-Opioid receptor (MOR) agonists represent the gold standard for the treatment of severe pain but may paradoxically also enhance pain sensitivity, that is, lead to opioid-induced hyperalgesia (OIH). We show that abrupt withdrawal from MOR agonists induces long-term potentiation (LTP) at the first synapse in pain pathways. Induction of opioid withdrawal LTP requires postsynaptic activation of heterotrimeric guanine nucleotide-binding proteins and N-methyl-d-aspartate receptors and a rise of postsynaptic calcium concentrations. In contrast, the acute depression by opioids is induced presynaptically at these synapses. Withdrawal LTP can be prevented by tapered withdrawal and shares pharmacology and signal transduction pathways with OIH. These findings provide a previously unrecognized target to selectively combat pro-nociceptive effects of opioids without compromising opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Drdla, Ruth -- Gassner, Matthias -- Gingl, Ewald -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2009 Jul 10;325(5937):207-10. doi: 10.1126/science.1171759.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19590003" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Opioid/administration & dosage/*adverse effects/pharmacology ; Animals ; Calcium/metabolism ; Enkephalin, Ala(2)-MePhe(4)-Gly(5)-/administration & dosage/adverse ; effects/pharmacology ; Evoked Potentials ; GTP-Binding Proteins/metabolism ; Hyperalgesia/chemically induced ; *Long-Term Potentiation/drug effects ; Male ; Nerve Fibers, Unmyelinated/physiology ; Patch-Clamp Techniques ; Piperidines/administration & dosage/adverse effects/pharmacology ; Posterior Horn Cells/drug effects/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Opioid, mu/*agonists ; Signal Transduction ; Substance Withdrawal Syndrome/*physiopathology ; Synapses/drug effects/*physiology
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  • 17
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    Energy-efficient action potentials in hippocampal mossy fibers (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-09-12
    Description: Action potentials in nonmyelinated axons are considered to contribute substantially to activity-dependent brain metabolism. Here we show that fast Na+ current decay and delayed K+ current onset during action potentials in nonmyelinated mossy fibers of the rat hippocampus minimize the overlap of their respective ion fluxes. This results in total Na+ influx and associated energy demand per action potential of only 1.3 times the theoretical minimum, in contrast to the factor of 4 used in previous energy budget calculations for neural activity. Analysis of ionic conductance parameters revealed that the properties of Na+ and K+ channels are matched to make axonal action potentials energy-efficient, minimizing their contribution to activity-dependent metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alle, Henrik -- Roth, Arnd -- Geiger, Jorg R P -- New York, N.Y. -- Science. 2009 Sep 11;325(5946):1405-8. doi: 10.1126/science.1174331.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Independent Hertie Research Group, Max-Planck-Institute for Brain Research, 60528 Frankfurt, Germany. henrik.alle@charite.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745156" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Axons/physiology ; *Energy Metabolism ; Mossy Fibers, Hippocampal/*physiology ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channels/metabolism ; Presynaptic Terminals/physiology ; Rats ; Rats, Wistar ; Sodium/metabolism ; Sodium Channels/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Synaptic Transmission
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  • 18
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    Norbin is an endogenous regulator of metabotropic glutamate receptor 5 signaling (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-17
    Description: Metabotropic glutamate receptor 5 (mGluR5) is highly expressed in the mammalian central nervous system (CNS). It is involved in multiple physiological functions and is a target for treatment of various CNS disorders, including schizophrenia. We report that Norbin, a neuron-specific protein, physically interacts with mGluR5 in vivo, increases the cell surface localization of the receptor, and positively regulates mGluR5 signaling. Genetic deletion of Norbin attenuates mGluR5-dependent stable changes in synaptic function measured as long-term depression or long-term potentiation of synaptic transmission in the hippocampus. As with mGluR5 knockout mice or mice treated with mGluR5-selective antagonists, Norbin knockout mice showed a behavioral phenotype associated with a rodent model of schizophrenia, as indexed by alterations both in sensorimotor gating and psychotomimetic-induced locomotor activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796550/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Hong -- Westin, Linda -- Nong, Yi -- Birnbaum, Shari -- Bendor, Jacob -- Brismar, Hjalmar -- Nestler, Eric -- Aperia, Anita -- Flajolet, Marc -- Greengard, Paul -- DA 10044/DA/NIDA NIH HHS/ -- MH074866/MH/NIMH NIH HHS/ -- MH66172/MH/NIMH NIH HHS/ -- P01 DA010044/DA/NIDA NIH HHS/ -- P01 DA010044-020002/DA/NIDA NIH HHS/ -- P01 DA010044-030002/DA/NIDA NIH HHS/ -- P01 DA010044-04/DA/NIDA NIH HHS/ -- P01 DA010044-040002/DA/NIDA NIH HHS/ -- P01 DA010044-05/DA/NIDA NIH HHS/ -- P01 DA010044-050002/DA/NIDA NIH HHS/ -- P01 DA010044-06/DA/NIDA NIH HHS/ -- P01 DA010044-060002/DA/NIDA NIH HHS/ -- P01 DA010044-07/DA/NIDA NIH HHS/ -- P01 DA010044-070002/DA/NIDA NIH HHS/ -- P01 DA010044-08/DA/NIDA NIH HHS/ -- P01 DA010044-080002/DA/NIDA NIH HHS/ -- P01 DA010044-09/DA/NIDA NIH HHS/ -- P01 DA010044-090002/DA/NIDA NIH HHS/ -- P01 DA010044-10/DA/NIDA NIH HHS/ -- P01 DA010044-100002/DA/NIDA NIH HHS/ -- P01 DA010044-11/DA/NIDA NIH HHS/ -- P01 DA010044-110005/DA/NIDA NIH HHS/ -- P01 DA010044-12/DA/NIDA NIH HHS/ -- P01 DA010044-120005/DA/NIDA NIH HHS/ -- P01 DA010044-129002/DA/NIDA NIH HHS/ -- P01 DA010044-13/DA/NIDA NIH HHS/ -- P01 DA010044-130005/DA/NIDA NIH HHS/ -- P01 DA010044-139002/DA/NIDA NIH HHS/ -- P01 DA010044-14/DA/NIDA NIH HHS/ -- P01 DA010044-140005/DA/NIDA NIH HHS/ -- P01 DA010044-149002/DA/NIDA NIH HHS/ -- P01 DA010044-14S1/DA/NIDA NIH HHS/ -- P01 DA010044-14S10005/DA/NIDA NIH HHS/ -- P01 DA010044-14S19002/DA/NIDA NIH HHS/ -- P50 MH074866/MH/NIMH NIH HHS/ -- P50 MH074866-010001/MH/NIMH NIH HHS/ -- P50 MH074866-020001/MH/NIMH NIH HHS/ -- P50 MH074866-030001/MH/NIMH NIH HHS/ -- P50 MH074866-039001/MH/NIMH NIH HHS/ -- P50 MH074866-040001/MH/NIMH NIH HHS/ -- P50 MH074866-050001/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Dec 11;326(5959):1554-7. doi: 10.1126/science.1178496.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20007903" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium Signaling ; Cell Line ; Cell Membrane/metabolism ; Humans ; Mice ; Mice, Knockout ; Motor Activity ; Nerve Tissue Proteins/genetics/*metabolism ; Neuronal Plasticity ; Protein Binding ; Rats ; Receptor, Metabotropic Glutamate 5 ; Receptors, Metabotropic Glutamate/genetics/*metabolism ; Reflex, Startle ; Schizophrenia/physiopathology ; *Signal Transduction ; Synaptic Transmission ; Transfection
    Print ISSN: 0036-8075
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    Spinal endocannabinoids and CB1 receptors mediate C-fiber-induced heterosynaptic pain sensitization (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Diminished synaptic inhibition in the spinal dorsal horn is a major contributor to chronic pain. Pathways that reduce synaptic inhibition in inflammatory and neuropathic pain states have been identified, but central hyperalgesia and diminished dorsal horn synaptic inhibition also occur in the absence of inflammation or neuropathy, solely triggered by intense nociceptive (C-fiber) input to the spinal dorsal horn. We found that endocannabinoids, produced upon strong nociceptive stimulation, activated type 1 cannabinoid (CB1) receptors on inhibitory dorsal horn neurons to reduce the synaptic release of gamma-aminobutyric acid and glycine and thus rendered nociceptive neurons excitable by nonpainful stimuli. Our results suggest that spinal endocannabinoids and CB1 receptors on inhibitory dorsal horn interneurons act as mediators of heterosynaptic pain sensitization and play an unexpected role in dorsal horn pain-controlling circuits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835775/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2835775/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pernia-Andrade, Alejandro J -- Kato, Ako -- Witschi, Robert -- Nyilas, Rita -- Katona, Istvan -- Freund, Tamas F -- Watanabe, Masahiko -- Filitz, Jorg -- Koppert, Wolfgang -- Schuttler, Jurgen -- Ji, Guangchen -- Neugebauer, Volker -- Marsicano, Giovanni -- Lutz, Beat -- Vanegas, Horacio -- Zeilhofer, Hanns Ulrich -- NS11255/NS/NINDS NIH HHS/ -- NS38261/NS/NINDS NIH HHS/ -- P01 NS011255/NS/NINDS NIH HHS/ -- P01 NS011255-32A20042/NS/NINDS NIH HHS/ -- P01 NS011255-330042/NS/NINDS NIH HHS/ -- R01 NS038261/NS/NINDS NIH HHS/ -- R01 NS038261-08/NS/NINDS NIH HHS/ -- R01 NS038261-09/NS/NINDS NIH HHS/ -- R01 NS038261-10/NS/NINDS NIH HHS/ -- R01 NS038261-10S1/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Aug 7;325(5941):760-4. doi: 10.1126/science.1171870.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Pharmacology and Toxicology, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661434" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Cannabinoid Receptor Modulators/*physiology ; Electric Stimulation ; *Endocannabinoids ; Excitatory Postsynaptic Potentials ; Female ; Humans ; Hyperalgesia/*physiopathology ; Inhibitory Postsynaptic Potentials ; Interneurons/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nerve Fibers, Unmyelinated/*physiology ; Neural Inhibition ; Pain/*physiopathology ; Piperidines/administration & dosage/pharmacology ; Posterior Horn Cells/*physiology ; Pyrazoles/administration & dosage/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/antagonists & inhibitors/*metabolism ; Spinal Cord/cytology/physiology ; *Synaptic Transmission ; Young Adult
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Comment on "Detection, stimulation, and inhibition of neuronal signals with high-density nanowire transistor arrays" (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-17
    Description: Patolsky et al. (Reports, 25 August 2006, p. 1100) used silicon nanowires to record action potentials in rat neuronal axons and found increases in conductance of about 85 nanosiemens. We point out that the data correspond to voltage changes of about -85 millivolts on the nanowire and that conceivable mechanisms of axon-nanowire interaction lead to signals that are opposite in sign or smaller by orders of magnitude.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fromherz, Peter -- Voelker, Moritz -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1429; author reply 1429. doi: 10.1126/science.1155416.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Membrane and Neurophysics, Max Planck Institute for Biochemistry, D82152 Martinsried/Munich, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19286538" target="_blank"〉PubMed〈/a〉
    Keywords: *Action Potentials ; Animals ; Axons/*physiology ; Electric Conductivity ; Electric Stimulation ; Ion Channel Gating ; *Nanowires ; Neural Inhibition ; Neurons/*physiology ; Rats ; Semiconductors ; Silicon ; Sodium/metabolism ; Static Electricity ; Transistors, Electronic
    Print ISSN: 0036-8075
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  • 21
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    A Cdc20-APC ubiquitin signaling pathway regulates presynaptic differentiation (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-11-11
    Description: Presynaptic axonal differentiation is essential for synapse formation and the establishment of neuronal circuits. However, the mechanisms that coordinate presynaptic development in the brain are largely unknown. We found that the major mitotic E3 ubiquitin ligase Cdc20-anaphase promoting complex (Cdc20-APC) regulates presynaptic differentiation in primary postmitotic mammalian neurons and in the rat cerebellar cortex. Cdc20-APC triggered the degradation of the transcription factor NeuroD2 and thereby promoted presynaptic differentiation. The NeuroD2 target gene encoding Complexin II, which acts locally at presynaptic sites, mediated the ability of NeuroD2 to suppress presynaptic differentiation. Thus, our findings define a Cdc20-APC ubiquitin signaling pathway that governs presynaptic development, which holds important implications for neuronal connectivity and plasticity in the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846784/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846784/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yang, Yue -- Kim, Albert H -- Yamada, Tomoko -- Wu, Bei -- Bilimoria, Parizad M -- Ikeuchi, Yoshiho -- de la Iglesia, Nuria -- Shen, Jie -- Bonni, Azad -- F32 CA124028/CA/NCI NIH HHS/ -- NS041021/NS/NINDS NIH HHS/ -- NS051255/NS/NINDS NIH HHS/ -- R01 NS041021/NS/NINDS NIH HHS/ -- R01 NS041021-06/NS/NINDS NIH HHS/ -- R01 NS041021-07/NS/NINDS NIH HHS/ -- R01 NS041021-08/NS/NINDS NIH HHS/ -- R01 NS051255/NS/NINDS NIH HHS/ -- R01 NS051255-02/NS/NINDS NIH HHS/ -- R01 NS051255-03/NS/NINDS NIH HHS/ -- R01 NS051255-04/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 23;326(5952):575-8. doi: 10.1126/science.1177087.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19900895" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Vesicular Transport/genetics/metabolism ; Anaphase-Promoting Complex-Cyclosome ; Animals ; Axons/metabolism/*physiology/ultrastructure ; Basic Helix-Loop-Helix Transcription Factors/genetics/metabolism ; Cdc20 Proteins ; Cell Cycle Proteins/genetics/*metabolism ; Cerebellar Cortex/cytology/metabolism/ultrastructure ; Gene Knockdown Techniques ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/genetics/metabolism ; Neuropeptides/genetics/metabolism ; Presynaptic Terminals/*metabolism ; Rats ; *Signal Transduction ; Synapses/*metabolism ; Synapsins/metabolism ; Synaptic Vesicles/genetics/metabolism ; Ubiquitin/*metabolism ; Ubiquitin-Protein Ligase Complexes/genetics/*metabolism ; Ubiquitin-Protein Ligases/*metabolism
    Print ISSN: 0036-8075
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  • 22
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    Spinal cord stimulation restores locomotion in animal models of Parkinson's disease (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-03-21
    Description: Dopamine replacement therapy is useful for treating motor symptoms in the early phase of Parkinson's disease, but it is less effective in the long term. Electrical deep-brain stimulation is a valuable complement to pharmacological treatment but involves a highly invasive surgical procedure. We found that epidural electrical stimulation of the dorsal columns in the spinal cord restores locomotion in both acute pharmacologically induced dopamine-depleted mice and in chronic 6-hydroxydopamine-lesioned rats. The functional recovery was paralleled by a disruption of aberrant low-frequency synchronous corticostriatal oscillations, leading to the emergence of neuronal activity patterns that resemble the state normally preceding spontaneous initiation of locomotion. We propose that dorsal column stimulation might become an efficient and less invasive alternative for treatment of Parkinson's disease in the future.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669752/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669752/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fuentes, Romulo -- Petersson, Per -- Siesser, William B -- Caron, Marc G -- Nicolelis, Miguel A L -- R21 NS049534/NS/NINDS NIH HHS/ -- R21 NS049534-01A2/NS/NINDS NIH HHS/ -- R21 NS049534-02/NS/NINDS NIH HHS/ -- R33 NS049534/NS/NINDS NIH HHS/ -- R33 NS049534-03/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 20;323(5921):1578-82. doi: 10.1126/science.1164901.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA. fuentes@neuro.duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299613" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways/physiology ; Animals ; Combined Modality Therapy ; Corpus Striatum/physiopathology ; Dopamine/metabolism ; *Electric Stimulation Therapy ; Electrodes, Implanted ; Electrophysiological Phenomena ; Humans ; Levodopa/administration & dosage/therapeutic use ; *Locomotion ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Cortex/physiopathology ; Neurons/physiology ; Oxidopamine/pharmacology ; Parkinson Disease/physiopathology/*therapy ; Parkinsonian Disorders/physiopathology/*therapy ; Rats ; Spinal Cord/*physiology ; alpha-Methyltyrosine/pharmacology
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    Neuroscience. Erasing fear memories (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pizzorusso, Tommaso -- New York, N.Y. -- Science. 2009 Sep 4;325(5945):1214-5. doi: 10.1126/science.1179697.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Istituto Neuroscienze CNR, via Moruzzi, 1 56100 Pisa, Italy. tommaso.pizzorusso@in.cnr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19729646" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/growth & development/*physiology ; Animals ; Chondroitin ABC Lyase/metabolism ; Chondroitin Sulfate Proteoglycans/metabolism/*physiology ; Conditioning, Classical ; *Extinction, Psychological ; Extracellular Matrix/physiology ; *Fear ; Memory/*physiology ; Mice ; Neuronal Plasticity ; Rats ; Visual Cortex/growth & development/physiology
    Print ISSN: 0036-8075
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  • 24
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    Synaptic integration in tuft dendrites of layer 5 pyramidal neurons: a new unifying principle (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-08-08
    Description: Tuft dendrites are the main target for feedback inputs innervating neocortical layer 5 pyramidal neurons, but their properties remain obscure. We report the existence of N-methyl-D-aspartate (NMDA) spikes in the fine distal tuft dendrites that otherwise did not support the initiation of calcium spikes. Both direct measurements and computer simulations showed that NMDA spikes are the dominant mechanism by which distal synaptic input leads to firing of the neuron and provide the substrate for complex parallel processing of top-down input arriving at the tuft. These data lead to a new unifying view of integration in pyramidal neurons in which all fine dendrites, basal and tuft, integrate inputs locally through the recruitment of NMDA receptor channels relative to the fixed apical calcium and axosomatic sodium integration points.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Larkum, Matthew E -- Nevian, Thomas -- Sandler, Maya -- Polsky, Alon -- Schiller, Jackie -- New York, N.Y. -- Science. 2009 Aug 7;325(5941):756-60. doi: 10.1126/science.1171958.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Berne, Buhlplatz 5, 3012 Berne, Switzerland. matthew.larkum@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19661433" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Calcium Signaling ; Computer Simulation ; Dendrites/*physiology ; Excitatory Postsynaptic Potentials ; In Vitro Techniques ; Models, Neurological ; N-Methylaspartate/metabolism ; Neocortex/cytology/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Sodium/metabolism ; Synapses/*physiology ; Synaptic Potentials
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    Neuroscience. Nuclear power for axonal growth (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subang, M C -- Richardson, P M -- New York, N.Y. -- Science. 2009 Oct 9;326(5950):238-9. doi: 10.1126/science.1181038.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bone and Joint Research, Barts and the London School of Medicine, Charterhouse Square, London EC1M 6BQ, UK. m.c.subang@qmul.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19815761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Cell Nucleus/*metabolism ; Cytoskeleton/metabolism ; Growth Cones/*physiology/ultrastructure ; Hippocampus/cytology/embryology ; Intercellular Signaling Peptides and Proteins/metabolism ; Kruppel-Like Transcription Factors/genetics/*metabolism ; Mice ; Nerve Regeneration ; Nerve Tissue Proteins/metabolism ; Rats ; Retinal Ganglion Cells/cytology ; Transcription Factors/metabolism ; Transcription, Genetic
    Print ISSN: 0036-8075
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  • 26
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    The dynamic control of kiss-and-run and vesicular reuse probed with single nanoparticles (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-02-14
    Description: Vesicular secretion of neurotransmitter is essential for neuronal communication. Kiss-and-run is a mode of membrane fusion and retrieval without the full collapse of the vesicle into the plasma membrane and de novo regeneration. The importance of kiss-and-run during efficient neurotransmission has remained in doubt. We developed an approach for loading individual synaptic vesicles with single quantum dots. Their size and pH-dependent photoluminescence change allowed us to distinguish kiss-and-run from full-collapse fusion and to track single vesicles through multiple rounds of kiss-and-run and reuse, without perturbing vesicle cycling. Kiss-and-run dominated at the beginning of stimulus trains, reflecting the preference of vesicles with high release probability. Its incidence was increased by rapid firing, a response appropriate to shape the kinetics of neurotransmission during a wide range of firing patterns.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696197/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696197/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Qi -- Li, Yulong -- Tsien, Richard W -- K99 DA025143/DA/NIDA NIH HHS/ -- K99 DA025143-01A1/DA/NIDA NIH HHS/ -- R01 MH064070/MH/NIMH NIH HHS/ -- R01 MH064070-08/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Mar 13;323(5920):1448-53. doi: 10.1126/science.1167373. Epub 2009 Feb 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19213879" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Electric Stimulation ; Hippocampus/cytology ; Hydrogen-Ion Concentration ; Ion Transport ; Luminescence ; *Membrane Fusion ; Neurons/*physiology ; Neurotransmitter Agents/metabolism ; Presynaptic Terminals/physiology ; Quantum Dots ; Rats ; Rats, Sprague-Dawley ; Synaptic Membranes/physiology ; *Synaptic Transmission ; Synaptic Vesicles/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 27
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    Rhes, a striatal specific protein, mediates mutant-huntingtin cytotoxicity (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-06-06
    Description: Huntington's disease (HD) is caused by a polyglutamine repeat in the protein huntingtin (Htt) with mutant Htt (mHtt) expressed throughout the body and similarly in all brain regions. Yet, HD neuropathology is largely restricted to the corpus striatum. We report that the small guanine nucleotide-binding protein Rhes, which is localized very selectively to the striatum, binds physiologically to mHtt. Using cultured cells, we found Rhes induces sumoylation of mHtt, which leads to cytotoxicity. Thus, Rhes-mHtt interactions can account for the localized neuropathology of HD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Subramaniam, Srinivasa -- Sixt, Katherine M -- Barrow, Roxanne -- Snyder, Solomon H -- DA00074/DA/NIDA NIH HHS/ -- MH18501/MH/NIMH NIH HHS/ -- R37 MH018501/MH/NIMH NIH HHS/ -- R37 MH018501-40/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Jun 5;324(5932):1327-30. doi: 10.1126/science.1172871.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19498170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Death ; Cell Line ; Cell Survival ; Corpus Striatum/metabolism ; GTP-Binding Proteins/*metabolism ; Humans ; Mice ; Mice, Transgenic ; Mutant Proteins/metabolism ; Nerve Tissue Proteins/chemistry/*metabolism ; Nuclear Proteins/chemistry/*metabolism ; PC12 Cells ; RNA Interference ; Rats ; Recombinant Fusion Proteins/metabolism ; SUMO-1 Protein/genetics/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Substrate Specificity
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    Role of layer 6 of V2 visual cortex in object-recognition memory (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-07-04
    Description: Cellular responses in the V2 secondary visual cortex to simple as well as complex visual stimuli have been well studied. However, the role of area V2 in visual memory remains unexplored. We found that layer 6 neurons of V2 are crucial for the processing of object-recognition memory (ORM). Using the protein regulator of G protein signaling-14 (RGS-14) as a tool, we found that the expression of this protein into layer 6 neurons of rat-brain area V2 promoted the conversion of a normal short-term ORM that normally lasts for 45 minutes into long-term memory detectable even after many months. Furthermore, elimination of the same-layer neurons by means of injection of a selective cytotoxin resulted in the complete loss of normal as well as protein-mediated enhanced ORM.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Aranda, Manuel F -- Lopez-Tellez, Juan F -- Navarro-Lobato, Irene -- Masmudi-Martin, Mariam -- Gutierrez, Antonia -- Khan, Zafar U -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):87-9. doi: 10.1126/science.1170869.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurobiology, Centro de Investigaciones Medico-Sanitarias, University of Malaga, Campus Teatinos s/n, 29071 Malaga, Spain. zkhan@uma.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574389" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Lentivirus/genetics ; Memory/*physiology ; Memory, Short-Term/*physiology ; Neurons/physiology ; RGS Proteins/genetics/metabolism ; Rats ; Rats, Wistar ; Recognition (Psychology)/*physiology ; Temporal Lobe/physiology ; Visual Cortex/cytology/*physiology ; Visual Perception
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    Translocator protein (18 kD) as target for anxiolytics without benzodiazepine-like side effects (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-06-23
    Description: Most antianxiety drugs (anxiolytics) work by modulating neurotransmitters in the brain. Benzodiazepines are fast and effective anxiolytic drugs; however, their long-term use is limited by the development of tolerance and withdrawal symptoms. Ligands of the translocator protein [18 kilodaltons (kD)] may promote the synthesis of endogenous neurosteroids, which also exert anxiolytic effects in animal models. Here, we found that the translocator protein (18 kD) ligand XBD173 enhanced gamma-aminobutyric acid-mediated neurotransmission and counteracted induced panic attacks in rodents in the absence of sedation and tolerance development. XBD173 also exerted antipanic activity in humans and, in contrast to benzodiazepines, did not cause sedation or withdrawal symptoms. Thus, translocator protein (18 kD) ligands are promising candidates for fast-acting anxiolytic drugs with less severe side effects than benzodiazepines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rupprecht, Rainer -- Rammes, Gerhard -- Eser, Daniela -- Baghai, Thomas C -- Schule, Cornelius -- Nothdurfter, Caroline -- Troxler, Thomas -- Gentsch, Conrad -- Kalkman, Hans O -- Chaperon, Frederique -- Uzunov, Veska -- McAllister, Kevin H -- Bertaina-Anglade, Valerie -- La Rochelle, Christophe Drieu -- Tuerck, Dietrich -- Floesser, Annette -- Kiese, Beate -- Schumacher, Michael -- Landgraf, Rainer -- Holsboer, Florian -- Kucher, Klaus -- New York, N.Y. -- Science. 2009 Jul 24;325(5939):490-3. doi: 10.1126/science.1175055. Epub 2009 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nussbaumstrasse 7, Munich 80336, Germany. rainer.rupprecht@med.uni-muenchen.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19541954" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Alprazolam/pharmacology ; Animals ; Anti-Anxiety Agents/adverse effects/*metabolism ; Benzodiazepines/adverse effects ; Cell Line ; Drug Tolerance ; Humans ; Isoquinolines/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Neurotransmitter Agents/metabolism ; Panic Disorder/drug therapy ; Purines/*therapeutic use ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA/*metabolism ; Receptors, GABA-A/metabolism ; Substance Withdrawal Syndrome/prevention & control ; Tetragastrin ; gamma-Aminobutyric Acid/metabolism
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    Neuroscience. More AMPAR garnish (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tigaret, Cezar -- Choquet, Daniel -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1295-6. doi: 10.1126/science.1171519.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UMR 5091 CNRS, Universite de Bordeaux, 146 rue Leo Saignat, 33077 Bordeaux Cedex, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19265005" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Brain/metabolism ; Caenorhabditis elegans Proteins/chemistry/metabolism ; Cell Membrane/metabolism ; Glutamic Acid/metabolism ; Kainic Acid/metabolism ; Membrane Proteins/chemistry/metabolism ; Neurons/*metabolism ; Rats ; Receptors, AMPA/chemistry/isolation & purification/*metabolism ; Synapses/metabolism ; *Synaptic Transmission
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    Optical deconstruction of parkinsonian neural circuitry (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-21
    Description: Deep brain stimulation (DBS) is a therapeutic option for intractable neurological and psychiatric disorders, including Parkinson's disease and major depression. Because of the heterogeneity of brain tissues where electrodes are placed, it has been challenging to elucidate the relevant target cell types or underlying mechanisms of DBS. We used optogenetics and solid-state optics to systematically drive or inhibit an array of distinct circuit elements in freely moving parkinsonian rodents and found that therapeutic effects within the subthalamic nucleus can be accounted for by direct selective stimulation of afferent axons projecting to this region. In addition to providing insight into DBS mechanisms, these results demonstrate an optical approach for dissection of disease circuitry and define the technological toolbox needed for systematic deconstruction of disease circuits by selectively controlling individual components.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gradinaru, Viviana -- Mogri, Murtaza -- Thompson, Kimberly R -- Henderson, Jaimie M -- Deisseroth, Karl -- New York, N.Y. -- Science. 2009 Apr 17;324(5925):354-9. doi: 10.1126/science.1167093. Epub 2009 Mar 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19299587" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Astrocytes/metabolism ; Axons/*physiology ; *Deep Brain Stimulation ; Fiber Optic Technology ; Halorhodopsins/metabolism ; Light ; Motor Activity ; Motor Cortex/pathology/physiopathology ; Neural Inhibition ; Neurons, Afferent/*physiology ; Optics and Photonics ; Parkinsonian Disorders/pathology/*physiopathology/therapy ; Rats ; Rhodopsin/metabolism ; Subthalamic Nucleus/pathology/*physiopathology
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    Neuroscience. Remembering outside the box (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-07-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Saksida, Lisa M -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):40-1. doi: 10.1126/science.1177156.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Experimental Psychology, University of Cambridge, Cambridge CB2 3EB, UK. lms42@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574374" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; Memory/*physiology ; RGS Proteins/metabolism ; Rats ; Recognition (Psychology)/*physiology ; Temporal Lobe/*physiology ; Visual Cortex/*physiology ; Visual Perception
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    Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6 (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-03
    Description: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease that is familial in 10% of cases. We have identified a missense mutation in the gene encoding fused in sarcoma (FUS) in a British kindred, linked to ALS6. In a survey of 197 familial ALS index cases, we identified two further missense mutations in eight families. Postmortem analysis of three cases with FUS mutations showed FUS-immunoreactive cytoplasmic inclusions and predominantly lower motor neuron degeneration. Cellular expression studies revealed aberrant localization of mutant FUS protein. FUS is involved in the regulation of transcription and RNA splicing and transport, and it has functional homology to another ALS gene, TARDBP, which suggests that a common mechanism may underlie motor neuron degeneration.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516382/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vance, Caroline -- Rogelj, Boris -- Hortobagyi, Tibor -- De Vos, Kurt J -- Nishimura, Agnes Lumi -- Sreedharan, Jemeen -- Hu, Xun -- Smith, Bradley -- Ruddy, Deborah -- Wright, Paul -- Ganesalingam, Jeban -- Williams, Kelly L -- Tripathi, Vineeta -- Al-Saraj, Safa -- Al-Chalabi, Ammar -- Leigh, P Nigel -- Blair, Ian P -- Nicholson, Garth -- de Belleroche, Jackie -- Gallo, Jean-Marc -- Miller, Christopher C -- Shaw, Christopher E -- 078662/Wellcome Trust/United Kingdom -- G0300329/Medical Research Council/United Kingdom -- G0500289/Medical Research Council/United Kingdom -- G0501573/Medical Research Council/United Kingdom -- G0600676/Medical Research Council/United Kingdom -- G0600974/Medical Research Council/United Kingdom -- G0900688/Medical Research Council/United Kingdom -- MC_G1000733/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2009 Feb 27;323(5918):1208-11. doi: 10.1126/science.1165942.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Clinical Neuroscience, King's College London, Medical Research Council (MRC) Centre for Neurodegeneration Research, Institute of Psychiatry, London SE5 8AF, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19251628" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Sequence ; Amyotrophic Lateral Sclerosis/*genetics/metabolism/pathology ; Animals ; Brain/pathology ; Cell Line ; Cell Nucleus/metabolism ; Cytoplasm/metabolism ; DNA-Binding Proteins/analysis/genetics/metabolism ; Female ; Humans ; Inclusion Bodies/chemistry/ultrastructure ; Male ; Molecular Sequence Data ; Motor Neurons/metabolism ; *Mutation, Missense ; Pedigree ; RNA-Binding Protein FUS/analysis/*genetics/*metabolism ; Rats ; Spinal Cord/pathology ; Transfection
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    Functional proteomics identify cornichon proteins as auxiliary subunits of AMPA receptors (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-03-07
    Description: Glutamate receptors of the AMPA-subtype (AMPARs), together with the transmembrane AMPAR regulatory proteins (TARPs), mediate fast excitatory synaptic transmission in the mammalian brain. Here, we show by proteomic analysis that the majority of AMPARs in the rat brain are coassembled with two members of the cornichon family of transmembrane proteins, rather than with the TARPs. Coassembly with cornichon homologs 2 and 3 affects AMPARs in two ways: Cornichons increase surface expression of AMPARs, and they alter channel gating by markedly slowing deactivation and desensitization kinetics. These results demonstrate that cornichons are intrinsic auxiliary subunits of native AMPARs and provide previously unknown molecular determinants for glutamatergic neurotransmission in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwenk, Jochen -- Harmel, Nadine -- Zolles, Gerd -- Bildl, Wolfgang -- Kulik, Akos -- Heimrich, Bernd -- Chisaka, Osamu -- Jonas, Peter -- Schulte, Uwe -- Fakler, Bernd -- Klocker, Nikolaj -- New York, N.Y. -- Science. 2009 Mar 6;323(5919):1313-9. doi: 10.1126/science.1167852.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology II, University of Freiburg, Engesserstrasse 4, 79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19265014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/*metabolism ; Cell Membrane/metabolism ; Glutamic Acid/metabolism ; Immunohistochemistry ; *Ion Channel Gating ; Kinetics ; Membrane Proteins/chemistry/metabolism ; Mice ; Neurons/*metabolism ; Patch-Clamp Techniques ; Protein Subunits/chemistry/metabolism ; Proteomics ; Rats ; Receptors, AMPA/chemistry/*metabolism ; Signal Transduction ; Synapses/metabolism ; *Synaptic Transmission ; Xenopus
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    GABAergic hub neurons orchestrate synchrony in developing hippocampal networks (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Brain function operates through the coordinated activation of neuronal assemblies. Graph theory predicts that scale-free topologies, which include "hubs" (superconnected nodes), are an effective design to orchestrate synchronization. Whether hubs are present in neuronal assemblies and coordinate network activity remains unknown. Using network dynamics imaging, online reconstruction of functional connectivity, and targeted whole-cell recordings in rats and mice, we found that developing hippocampal networks follow a scale-free topology, and we demonstrated the existence of functional hubs. Perturbation of a single hub influenced the entire network dynamics. Morphophysiological analysis revealed that hub cells are a subpopulation of gamma-aminobutyric acid-releasing (GABAergic) interneurons possessing widespread axonal arborizations. These findings establish a central role for GABAergic interneurons in shaping developing networks and help provide a conceptual framework for studying neuronal synchrony.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonifazi, P -- Goldin, M -- Picardo, M A -- Jorquera, I -- Cattani, A -- Bianconi, G -- Represa, A -- Ben-Ari, Y -- Cossart, R -- New York, N.Y. -- Science. 2009 Dec 4;326(5958):1419-24. doi: 10.1126/science.1175509.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Neurobiologie de la Mediterranee INSERM U901, Universitede la Mediterranee, Parc Scientifique de Luminy, Boite Postale 13, 13273 Marseille Cedex 9, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965761" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/ultrastructure ; CA3 Region, Hippocampal/cytology/*physiology ; Calcium/metabolism ; Dendrites/ultrastructure ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/*physiology/ultrastructure ; Mice ; Nerve Net/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Rats ; Rats, Wistar ; Synapses/physiology ; gamma-Aminobutyric Acid/*physiology
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    Neuroscience. Low-cost travel in neurons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magistretti, Pierre J -- New York, N.Y. -- Science. 2009 Sep 11;325(5946):1349-51. doi: 10.1126/science.1180102.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL), Switzerland. pierre.magistretti@epfl.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19745140" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Astrocytes/physiology ; Axons/physiology ; Brain/*physiology ; *Energy Metabolism ; *Excitatory Postsynaptic Potentials ; Glucose/metabolism ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; Humans ; Neurons/*physiology ; Neurotransmitter Agents/metabolism ; Potassium Channels/metabolism ; Rats ; Sodium Channels/metabolism ; Synapses/physiology ; Synaptic Transmission
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    Functional amyloids as natural storage of peptide hormones in pituitary secretory granules (2009)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2009-06-23
    Description: Amyloids are highly organized cross-beta-sheet-rich protein or peptide aggregates that are associated with pathological conditions including Alzheimer's disease and type II diabetes. However, amyloids may also have a normal biological function, as demonstrated by fungal prions, which are involved in prion replication, and the amyloid protein Pmel17, which is involved in mammalian skin pigmentation. We found that peptide and protein hormones in secretory granules of the endocrine system are stored in an amyloid-like cross-beta-sheet-rich conformation. Thus, functional amyloids in the pituitary and other organs can contribute to normal cell and tissue physiology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865899/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865899/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maji, Samir K -- Perrin, Marilyn H -- Sawaya, Michael R -- Jessberger, Sebastian -- Vadodaria, Krishna -- Rissman, Robert A -- Singru, Praful S -- Nilsson, K Peter R -- Simon, Rozalyn -- Schubert, David -- Eisenberg, David -- Rivier, Jean -- Sawchenko, Paul -- Vale, Wylie -- Riek, Roland -- P01 DK026741/DK/NIDDK NIH HHS/ -- P01 DK026741-29/DK/NIDDK NIH HHS/ -- P01 DK026741-30/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2009 Jul 17;325(5938):328-32. doi: 10.1126/science.1173155. Epub 2009 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Physical Chemistry, Eidgenossische Technische Hochschule (ETH) Zurich, Wolfgang-Paulistrasse 10, CH-8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19541956" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/chemistry/metabolism ; Amyloid/*chemistry/metabolism ; Animals ; Cell Survival ; Corticotropin-Releasing Hormone/chemistry/metabolism ; Heparin, Low-Molecular-Weight/chemistry ; Humans ; Hydrogen-Ion Concentration ; Mice ; Neurons/cytology/physiology ; Peptide Hormones/*chemistry/metabolism ; Pituitary Gland/*chemistry ; Pituitary Gland, Anterior/chemistry/metabolism ; Pituitary Gland, Posterior/chemistry/metabolism ; Pituitary Hormones/*chemistry/metabolism ; Protein Conformation ; Rats ; Secretory Vesicles/*chemistry/metabolism ; Sheep ; Urocortins/chemistry/metabolism ; beta-Endorphin/chemistry/metabolism
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    Dendritic mechanisms underlying rapid synaptic activation of fast-spiking hippocampal interneurons (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-12-08
    Description: Fast-spiking, parvalbumin-expressing basket cells (BCs) are important for feedforward and feedback inhibition. During network activity, BCs respond with short latency and high temporal precision. It is thought that the specific properties of input synapses are responsible for rapid recruitment. However, a potential contribution of active dendritic conductances has not been addressed. We combined confocal imaging and patch-clamp techniques to obtain simultaneous somatodendritic recordings from BCs. Action potentials were initiated in the BC axon and backpropagated into the dendrites with reduced amplitude and little activity dependence. These properties were explained by a high K+ to Na+ conductance ratio in BC dendrites. Computational analysis indicated that dendritic K+ channels convey unique integration properties to BCs, leading to the rapid and temporally precise activation by excitatory inputs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Hua -- Martina, Marco -- Jonas, Peter -- New York, N.Y. -- Science. 2010 Jan 1;327(5961):52-8. doi: 10.1126/science.1177876. Epub 2009 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology I, Universitat Freiburg, Engesserstrasse 4, D-79108 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19965717" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Dendrites/*physiology ; Dentate Gyrus/cytology/*physiology ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/*physiology ; Ion Channel Gating ; Microscopy, Confocal ; Neural Inhibition ; Parvalbumins/metabolism ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channels, Voltage-Gated/metabolism ; Rats ; Rats, Wistar ; Sodium/metabolism ; Sodium Channels/metabolism ; Synapses/*physiology ; Synaptic Transmission
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    Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-03-01
    Description: Long-term potentiation (LTP) at glutamatergic synapses is considered to underlie learning and memory and is associated with the enlargement of dendritic spines. Because the consolidation of memory and LTP require protein synthesis, it is important to clarify how protein synthesis affects spine enlargement. In rat brain slices, the repetitive pairing of postsynaptic spikes and two-photon uncaging of glutamate at single spines (a spike-timing protocol) produced both immediate and gradual phases of spine enlargement in CA1 pyramidal neurons. The gradual enlargement was strongly dependent on protein synthesis and brain-derived neurotrophic factor (BDNF) action, often associated with spine twitching, and was induced specifically at the spines that were immediately enlarged by the synaptic stimulation. Thus, this spike-timing protocol is an efficient trigger for BDNF secretion and induces protein synthesis-dependent long-term enlargement at the level of single spines.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4218863/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4218863/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanaka, Jun-Ichi -- Horiike, Yoshihiro -- Matsuzaki, Masanori -- Miyazaki, Takashi -- Ellis-Davies, Graham C R -- Kasai, Haruo -- R01 GM053395/GM/NIGMS NIH HHS/ -- R01 GM053395-12/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1683-7. doi: 10.1126/science.1152864. Epub 2008 Feb 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Structural Physiology, Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18309046" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain-Derived Neurotrophic Factor/*metabolism/pharmacology ; Cells, Cultured ; Dendritic Spines/*physiology/*ultrastructure ; Glutamic Acid/metabolism ; *Neuronal Plasticity ; Patch-Clamp Techniques ; *Protein Biosynthesis ; Protein Synthesis Inhibitors/pharmacology ; Pyramidal Cells/physiology/ultrastructure ; Rats ; Rats, Sprague-Dawley ; Receptor, trkB/metabolism ; Synapses/*physiology
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    Design logic of a cannabinoid receptor signaling network that triggers neurite outgrowth (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-05-20
    Description: Cannabinoid receptor 1 (CB1R) regulates neuronal differentiation. To understand the logic underlying decision-making in the signaling network controlling CB1R-induced neurite outgrowth, we profiled the activation of several hundred transcription factors after cell stimulation. We assembled an in silico signaling network by connecting CB1R to 23 activated transcription factors. Statistical analyses of this network predicted a role for the breast cancer 1 protein BRCA1 in neuronal differentiation and a new pathway from CB1R through phosphoinositol 3-kinase to the transcription factor paired box 6 (PAX6). Both predictions were experimentally confirmed. Results of transcription factor activation experiments that used pharmacological inhibitors of kinases revealed a network organization of partial OR gates regulating kinases stacked above AND gates that control transcription factors, which together allow for distributed decision-making in CB1R-induced neurite outgrowth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776723/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776723/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bromberg, Kenneth D -- Ma'ayan, Avi -- Neves, Susana R -- Iyengar, Ravi -- 1 S10 RR0 9145-01/RR/NCRR NIH HHS/ -- 5R24 CA095823-04/CA/NCI NIH HHS/ -- GM072853/GM/NIGMS NIH HHS/ -- GM54508/GM/NIGMS NIH HHS/ -- P50 GM071558/GM/NIGMS NIH HHS/ -- P50 GM071558-01A2/GM/NIGMS NIH HHS/ -- P50 GM071558-01A20007/GM/NIGMS NIH HHS/ -- P50 GM071558-02/GM/NIGMS NIH HHS/ -- P50 GM071558-020007/GM/NIGMS NIH HHS/ -- P50 GM071558-030007/GM/NIGMS NIH HHS/ -- P50-071558/PHS HHS/ -- R01 GM054508/GM/NIGMS NIH HHS/ -- R01 GM054508-21/GM/NIGMS NIH HHS/ -- R01 GM072853/GM/NIGMS NIH HHS/ -- R01 GM072853-04/GM/NIGMS NIH HHS/ -- T32 CA88796/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 May 16;320(5878):903-9. doi: 10.1126/science.1152662.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18487186" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cell Differentiation ; Cell Line, Tumor ; Cells, Cultured ; Computational Biology ; Computer Simulation ; Eye Proteins/metabolism ; Hippocampus/cytology ; Homeodomain Proteins/metabolism ; Metabolic Networks and Pathways ; Mice ; Neurites/*physiology ; Neurons/*cytology/metabolism ; Paired Box Transcription Factors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Interaction Mapping ; Rats ; Receptor, Cannabinoid, CB1/*metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; Transcription Factors/antagonists & inhibitors/*metabolism
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    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-08
    Description: We report that developmental competition between sympathetic neurons for survival is critically dependent on a sensitization process initiated by target innervation and mediated by a series of feedback loops. Target-derived nerve growth factor (NGF) promoted expression of its own receptor TrkA in mouse and rat neurons and prolonged TrkA-mediated signals. NGF also controlled expression of brain-derived neurotrophic factor and neurotrophin-4, which, through the receptor p75, can kill neighboring neurons with low retrograde NGF-TrkA signaling whereas neurons with high NGF-TrkA signaling are protected. Perturbation of any of these feedback loops disrupts the dynamics of competition. We suggest that three target-initiated events are essential for rapid and robust competition between neurons: sensitization, paracrine apoptotic signaling, and protection from such effects.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deppmann, Christopher D -- Mihalas, Stefan -- Sharma, Nikhil -- Lonze, Bonnie E -- Niebur, Ernst -- Ginty, David D -- EY016281/EY/NEI NIH HHS/ -- F32 NS053187/NS/NINDS NIH HHS/ -- NS053187/NS/NINDS NIH HHS/ -- NS34814/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):369-73. doi: 10.1126/science.1152677. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Solomon Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323418" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Apoptosis ; Brain-Derived Neurotrophic Factor/metabolism ; Cell Survival ; Cells, Cultured ; Computer Simulation ; Feedback, Physiological ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Mathematics ; Mice ; *Models, Neurological ; Nerve Growth Factor/*metabolism ; Nerve Growth Factors/metabolism ; Neurons/cytology/*physiology ; Oligonucleotide Array Sequence Analysis ; Rats ; Receptor, trkA/genetics/*metabolism ; Receptors, Nerve Growth Factor/genetics/metabolism ; Signal Transduction ; Superior Cervical Ganglion/*cytology
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    Internally generated cell assembly sequences in the rat hippocampus (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: A long-standing conjecture in neuroscience is that aspects of cognition depend on the brain's ability to self-generate sequential neuronal activity. We found that reliably and continually changing cell assemblies in the rat hippocampus appeared not only during spatial navigation but also in the absence of changing environmental or body-derived inputs. During the delay period of a memory task, each moment in time was characterized by the activity of a particular assembly of neurons. Identical initial conditions triggered a similar assembly sequence, whereas different conditions gave rise to different sequences, thereby predicting behavioral choices, including errors. Such sequences were not formed in control (nonmemory) tasks. We hypothesize that neuronal representations, evolved for encoding distance in spatial navigation, also support episodic recall and the planning of action sequences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570043/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570043/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pastalkova, Eva -- Itskov, Vladimir -- Amarasingham, Asohan -- Buzsaki, Gyorgy -- MH54671/MH/NIMH NIH HHS/ -- NS34994/NS/NINDS NIH HHS/ -- R01 MH054671/MH/NIMH NIH HHS/ -- R01 MH054671-10/MH/NIMH NIH HHS/ -- R01 NS034994/NS/NINDS NIH HHS/ -- R01 NS034994-11/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1322-7. doi: 10.1126/science.1159775.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Behavioral Neuroscience, Rutgers, State University of New Jersey, 197 University Avenue, Newark, NJ 07102, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772431" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Behavior, Animal ; Choice Behavior ; Cues ; Hippocampus/*cytology/*physiology ; Interneurons/physiology ; Male ; Maze Learning ; *Memory ; *Mental Recall ; Models, Neurological ; Motor Activity ; Pyramidal Cells/*physiology ; Rats ; Rats, Long-Evans
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    Neuroscience. The scale of experience (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-07-05
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590634/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2590634/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasselmo, Michael E -- DA16454/DA/NIDA NIH HHS/ -- MH60013/MH/NIMH NIH HHS/ -- MH60450/MH/NIMH NIH HHS/ -- MH61492/MH/NIMH NIH HHS/ -- MH71702/MH/NIMH NIH HHS/ -- P50 MH060450/MH/NIMH NIH HHS/ -- P50 MH060450-069002/MH/NIMH NIH HHS/ -- P50 MH060450-099002/MH/NIMH NIH HHS/ -- P50 MH071702/MH/NIMH NIH HHS/ -- P50 MH071702-030004/MH/NIMH NIH HHS/ -- R01 DA016454/DA/NIDA NIH HHS/ -- R01 DA016454-05/DA/NIDA NIH HHS/ -- R01 MH060013/MH/NIMH NIH HHS/ -- R01 MH060013-09/MH/NIMH NIH HHS/ -- R01 MH061492/MH/NIMH NIH HHS/ -- R01 MH061492-06A2/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2008 Jul 4;321(5885):46-7. doi: 10.1126/science.1160121.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Memory and Brain, Department of Psychology and Program in Neuroscience, Boston University, Boston, MA 02215, USA. hasselmo@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18599761" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Entorhinal Cortex/physiology ; Hippocampus/*cytology/*physiology ; Learning ; Membrane Potentials ; Models, Neurological ; Neurons/*physiology ; Rats ; *Space Perception ; Spatial Behavior
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    Neuroscience. Refreshing connections (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Silver, R Angus -- Kanichay, Roby T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):183-4. doi: 10.1126/science.1157589.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Physiology and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK. a.silver@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Diffusion ; *Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; *Neuronal Plasticity ; Rats ; Receptors, AMPA/*metabolism ; Synapses/*physiology ; *Synaptic Transmission ; Synaptic Vesicles/metabolism
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    Immunology. The toll of cathepsin K deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Krieg, Arthur M -- Lipford, Grayson B -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):576-7. doi: 10.1126/science.1154207.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Coley Pharmaceutical Group, 93 Worcester Street, Wellesley, MA 02481, USA. akrieg@coleypharma.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239112" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/*immunology/metabolism ; Cathepsin K ; Cathepsins/antagonists & inhibitors/deficiency/*metabolism ; Cytokines/secretion ; DNA, Bacterial/metabolism ; DNA, Viral/metabolism ; Dendritic Cells/immunology ; Dinucleoside Phosphates/immunology/metabolism ; Endoplasmic Reticulum/metabolism ; Endosomes/metabolism ; Humans ; *Immunity, Innate ; Inflammation/*immunology/metabolism ; Lysosomes/metabolism ; Mice ; Protease Inhibitors/pharmacology ; Rats ; Signal Transduction ; Toll-Like Receptor 9/antagonists & inhibitors/*metabolism
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    Leiomodin is an actin filament nucleator in muscle cells (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: Initiation of actin polymerization in cells requires nucleation factors. Here we describe an actin-binding protein, leiomodin, that acted as a strong filament nucleator in muscle cells. Leiomodin shared two actin-binding sites with the filament pointed end-capping protein tropomodulin: a flexible N-terminal region and a leucine-rich repeat domain. Leiomodin also contained a C-terminal extension of 150 residues. The smallest fragment with strong nucleation activity included the leucine-rich repeat and C-terminal extension. The N-terminal region enhanced the nucleation activity threefold and recruited tropomyosin, which weakly stimulated nucleation and mediated localization of leiomodin to the middle of muscle sarcomeres. Knocking down leiomodin severely compromised sarcomere assembly in cultured muscle cells, which suggests a role for leiomodin in the nucleation of tropomyosin-decorated filaments in muscles.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845909/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845909/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chereau, David -- Boczkowska, Malgorzata -- Skwarek-Maruszewska, Aneta -- Fujiwara, Ikuko -- Hayes, David B -- Rebowski, Grzegorz -- Lappalainen, Pekka -- Pollard, Thomas D -- Dominguez, Roberto -- GM026338/GM/NIGMS NIH HHS/ -- GM073791/GM/NIGMS NIH HHS/ -- HL086655/HL/NHLBI NIH HHS/ -- P01 HL086655/HL/NHLBI NIH HHS/ -- P01 HL086655-01A10004/HL/NHLBI NIH HHS/ -- R01 GM073791/GM/NIGMS NIH HHS/ -- R01 GM073791-04/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):239-43. doi: 10.1126/science.1155313.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boston Biomedical Research Institute, Watertown, MA 02472, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403713" target="_blank"〉PubMed〈/a〉
    Keywords: Actin Cytoskeleton/*metabolism ; Actins/metabolism ; Amino Acid Sequence ; Animals ; Binding Sites ; Cells, Cultured ; Cytoskeletal Proteins/chemistry/*metabolism ; Humans ; Microfilament Proteins/chemistry/*metabolism ; Molecular Sequence Data ; Muscle Proteins/chemistry/*metabolism ; Myocytes, Cardiac/*metabolism ; Protein Structure, Tertiary ; RNA Interference ; Rabbits ; Rats ; Sarcomeres/*metabolism ; Tropomodulin/chemistry ; Tropomyosin/chemistry/metabolism
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    Bioactive contaminants leach from disposable laboratory plasticware (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-08
    Description: Disposable plasticware such as test tubes, pipette tips, and multiwell assay or culture plates are used routinely in most biological research laboratories. Manufacturing of plastics requires the inclusion of numerous chemicals to enhance stability, durability, and performance. Some lubricating (slip) agents, exemplified by oleamide, also occur endogenously in humans and are biologically active, and cationic biocides are included to prevent bacterial colonization of the plastic surface. We demonstrate that these manufacturing agents leach from laboratory plasticware into a standard aqueous buffer, dimethyl sulfoxide, and methanol and can have profound effects on proteins and thus on results from bioassays of protein function. These findings have far-reaching implications for the use of disposable plasticware in biological research.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McDonald, G Reid -- Hudson, Alan L -- Dunn, Susan M J -- You, Haitao -- Baker, Glen B -- Whittal, Randy M -- Martin, Jonathan W -- Jha, Amitabh -- Edmondson, Dale E -- Holt, Andrew -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):917. doi: 10.1126/science.1162395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Alberta, Edmonton, AB T6G 2B7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dimethyl Sulfoxide ; Disinfectants/*analysis/pharmacology ; *Disposable Equipment ; Humans ; *Laboratories ; Monoamine Oxidase/*metabolism ; Monoamine Oxidase Inhibitors/pharmacology ; Oleic Acids/*analysis/pharmacology ; Plastics/*chemistry ; Quaternary Ammonium Compounds/*analysis/pharmacology ; Rats ; Solvents
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    Neuroscience. Hippocampal firing patterns linked to memory recall (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1280-1. doi: 10.1126/science.321.5894.1280b.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772404" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electrophysiology ; Epilepsy/*physiopathology/surgery ; Hippocampus/cytology/*physiology ; Humans ; Maze Learning ; Memory ; *Mental Recall ; Neurons/*physiology ; Rats
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  • 49
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    Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-05-24
    Description: Nitric oxide acts substantially in cellular signal transduction through stimulus-coupled S-nitrosylation of cysteine residues. The mechanisms that might subserve protein denitrosylation in cellular signaling remain uncharacterized. Our search for denitrosylase activities focused on caspase-3, an exemplar of stimulus-dependent denitrosylation, and identified thioredoxin and thioredoxin reductase in a biochemical screen. In resting human lymphocytes, thioredoxin-1 actively denitrosylated cytosolic caspase-3 and thereby maintained a low steady-state amount of S-nitrosylation. Upon stimulation of Fas, thioredoxin-2 mediated denitrosylation of mitochondria-associated caspase-3, a process required for caspase-3 activation, and promoted apoptosis. Inhibition of thioredoxin-thioredoxin reductases enabled identification of additional substrates subject to endogenous S-nitrosylation. Thus, specific enzymatic mechanisms may regulate basal and stimulus-induced denitrosylation in mammalian cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754768/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754768/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Benhar, Moran -- Forrester, Michael T -- Hess, Douglas T -- Stamler, Jonathan S -- P01 HL075443/HL/NHLBI NIH HHS/ -- P01 HL075443-050003/HL/NHLBI NIH HHS/ -- R01 HL059130/HL/NHLBI NIH HHS/ -- R01 HL059130-11/HL/NHLBI NIH HHS/ -- U19 ES012496/ES/NIEHS NIH HHS/ -- U19 ES012496-05/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 2008 May 23;320(5879):1050-4. doi: 10.1126/science.1158265.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18497292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD95/metabolism ; Apoptosis ; Auranofin/pharmacology ; Binding Sites ; Caspase 3/metabolism ; Caspase Inhibitors ; Cell Line ; Cytosol/*metabolism ; Dinitrochlorobenzene/pharmacology ; HeLa Cells ; Humans ; Jurkat Cells ; Macrophages/metabolism ; Mitochondria/enzymology/*metabolism ; Mitochondrial Proteins/*metabolism ; Nitric Oxide/*metabolism ; Rats ; Recombinant Proteins/metabolism ; S-Nitrosothiols/*metabolism ; T-Lymphocytes/metabolism ; Thioredoxin-Disulfide Reductase/*metabolism ; Thioredoxins/*metabolism
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    Reward-predictive cues enhance excitatory synaptic strength onto midbrain dopamine neurons (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-09-20
    Description: Using sensory information for the prediction of future events is essential for survival. Midbrain dopamine neurons are activated by environmental cues that predict rewards, but the cellular mechanisms that underlie this phenomenon remain elusive. We used in vivo voltammetry and in vitro patch-clamp electrophysiology to show that both dopamine release to reward predictive cues and enhanced synaptic strength onto dopamine neurons develop over the course of cue-reward learning. Increased synaptic strength was not observed after stable behavioral responding. Thus, enhanced synaptic strength onto dopamine neurons may act to facilitate the transformation of neutral environmental stimuli to salient reward-predictive cues.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613864/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2613864/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stuber, Garret D -- Klanker, Marianne -- de Ridder, Bram -- Bowers, M Scott -- Joosten, Ruud N -- Feenstra, Matthijs G -- Bonci, Antonello -- DA015096/DA/NIDA NIH HHS/ -- DA021937/DA/NIDA NIH HHS/ -- R01 DA015096/DA/NIDA NIH HHS/ -- R01 DA015096-06/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 19;321(5896):1690-2. doi: 10.1126/science.1160873.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ernest Gallo Clinic and Research Center, Department of Neurology, University of California, San Francisco, Emeryville, CA 94608, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18802002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Cues ; Dopamine/*physiology ; Excitatory Postsynaptic Potentials ; *Learning ; Long-Term Potentiation ; Male ; Mesencephalon/cytology/*physiology ; Neurons/*physiology ; Nucleus Accumbens/*physiology ; Patch-Clamp Techniques ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; *Reward ; Signal Transduction ; Synapses/*physiology ; Synaptic Transmission
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  • 51
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    Episodic-like memory in rats: is it based on when or how long ago? (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-05
    Description: Recent experiments with rats suggest that they show episodic-like or what-where-when memory for a preferred food found on a radial maze. Although memory for when a salient event occurred suggests that rats can mentally travel in time to a moment in the past, an alternative possibility is that they remember how long ago the food was found. Three groups of rats were tested for memory of previously encountered food. The different groups could use only the cues of when, how long ago, or when + how long ago. Only the cue of how long ago food was encountered was used successfully. These results suggest that episodic-like memory in rats is qualitatively different from human episodic memory.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, William A -- Feeney, Miranda C -- Macpherson, Krista -- Petter, Mark -- McMillan, Neil -- Musolino, Evanya -- New York, N.Y. -- Science. 2008 Apr 4;320(5872):113-5. doi: 10.1126/science.1152709.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Western Ontario, London, Ontario, N6A 5C2, Canada. roberts@uwo.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18388296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cues ; Male ; Maze Learning ; *Memory ; Random Allocation ; Rats ; Rats, Long-Evans ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Identifying autism loci and genes by tracing recent shared ancestry (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-16
    Description: To find inherited causes of autism-spectrum disorders, we studied families in which parents share ancestors, enhancing the role of inherited factors. We mapped several loci, some containing large, inherited, homozygous deletions that are likely mutations. The largest deletions implicated genes, including PCDH10 (protocadherin 10) and DIA1 (deleted in autism1, or c3orf58), whose level of expression changes in response to neuronal activity, a marker of genes involved in synaptic changes that underlie learning. A subset of genes, including NHE9 (Na+/H+ exchanger 9), showed additional potential mutations in patients with unrelated parents. Our findings highlight the utility of "homozygosity mapping" in heterogeneous disorders like autism but also suggest that defective regulation of gene expression after neural activity may be a mechanism common to seemingly diverse autism mutations.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586171/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2586171/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morrow, Eric M -- Yoo, Seung-Yun -- Flavell, Steven W -- Kim, Tae-Kyung -- Lin, Yingxi -- Hill, Robert Sean -- Mukaddes, Nahit M -- Balkhy, Soher -- Gascon, Generoso -- Hashmi, Asif -- Al-Saad, Samira -- Ware, Janice -- Joseph, Robert M -- Greenblatt, Rachel -- Gleason, Danielle -- Ertelt, Julia A -- Apse, Kira A -- Bodell, Adria -- Partlow, Jennifer N -- Barry, Brenda -- Yao, Hui -- Markianos, Kyriacos -- Ferland, Russell J -- Greenberg, Michael E -- Walsh, Christopher A -- 1K01MH71801/MH/NIMH NIH HHS/ -- 1K23MH080954-01/MH/NIMH NIH HHS/ -- 1R01 MH083565/MH/NIMH NIH HHS/ -- 5P30HD018655-26/HD/NICHD NIH HHS/ -- 5R01NS048276-05/NS/NINDS NIH HHS/ -- K01 MH071801/MH/NIMH NIH HHS/ -- K01 MH071801-04/MH/NIMH NIH HHS/ -- K01 MH071801-05/MH/NIMH NIH HHS/ -- K23 MH080954/MH/NIMH NIH HHS/ -- K23 MH080954-01/MH/NIMH NIH HHS/ -- MH64547/MH/NIMH NIH HHS/ -- N01-HG-65403/HG/NHGRI NIH HHS/ -- R01 MH083565/MH/NIMH NIH HHS/ -- R01 NS048276/NS/NINDS NIH HHS/ -- R01 NS048276-01/NS/NINDS NIH HHS/ -- R01 NS048276-02/NS/NINDS NIH HHS/ -- R01 NS048276-03/NS/NINDS NIH HHS/ -- R01 NS048276-04/NS/NINDS NIH HHS/ -- R01 NS048276-05/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 11;321(5886):218-23. doi: 10.1126/science.1157657.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Genetics, Children's Hospital Boston and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18621663" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics ; Animals ; Autistic Disorder/*genetics/physiopathology ; Brain/metabolism ; Cadherins/genetics ; *Chromosome Mapping ; Consanguinity ; Female ; Gene Deletion ; Gene Dosage ; Gene Expression Regulation ; Genes, Recessive ; Genetic Predisposition to Disease ; Homozygote ; Humans ; Lod Score ; Male ; *Mutation ; Neurons/physiology ; Oligonucleotide Array Sequence Analysis ; Pedigree ; Polymorphism, Single Nucleotide ; Rats ; Sodium-Hydrogen Antiporter/genetics ; Transcription Factors/genetics/metabolism
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    Electric fields due to synaptic currents sharpen excitatory transmission (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: The synaptic response waveform, which determines signal integration properties in the brain, depends on the spatiotemporal profile of neurotransmitter in the synaptic cleft. Here, we show that electrophoretic interactions between AMPA receptor-mediated excitatory currents and negatively charged glutamate molecules accelerate the clearance of glutamate from the synaptic cleft, speeding up synaptic responses. This phenomenon is reversed upon depolarization and diminished when intracleft electric fields are weakened through a decrease in the AMPA receptor density. In contrast, the kinetics of receptor-mediated currents evoked by direct application of glutamate are voltage-independent, as are synaptic currents mediated by the electrically neutral neurotransmitter GABA. Voltage-dependent temporal tuning of excitatory synaptic responses may thus contribute to signal integration in neural circuits.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685065/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685065/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sylantyev, Sergiy -- Savtchenko, Leonid P -- Niu, Yin-Ping -- Ivanov, Anton I -- Jensen, Thomas P -- Kullmann, Dimitri M -- Xiao, Min-Yi -- Rusakov, Dmitri A -- 071179/Wellcome Trust/United Kingdom -- G0400627/Medical Research Council/United Kingdom -- G0400627(71256)/Medical Research Council/United Kingdom -- G0400627(76527)/Medical Research Council/United Kingdom -- G0600368/Medical Research Council/United Kingdom -- G0600368(77987)/Medical Research Council/United Kingdom -- G116/147/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1845-9. doi: 10.1126/science.1154330.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurology, University College London, Queen Square, London, WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369150" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendrites/physiology ; Diffusion ; Dipeptides/pharmacology ; *Excitatory Postsynaptic Potentials ; Glutamic Acid/*metabolism ; Magnesium/pharmacology ; Male ; Monte Carlo Method ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Quinoxalines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/antagonists & inhibitors/*metabolism ; Receptors, GABA/metabolism ; Synapses/*physiology ; gamma-Aminobutyric Acid/metabolism
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  • 54
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    Activation of pannexin-1 hemichannels augments aberrant bursting in the hippocampus (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Pannexin-1 (Px1) is expressed at postsynaptic sites in pyramidal neurons, suggesting that these hemichannels contribute to dendritic signals associated with synaptic function. We found that, in pyramidal neurons, N-methyl-d-aspartate receptor (NMDAR) activation induced a secondary prolonged current and dye flux that were blocked with a specific inhibitory peptide against Px1 hemichannels; knockdown of Px1 by RNA interference blocked the current in cultured neurons. Enhancing endogenous NMDAR activation in brain slices by removing external magnesium ions (Mg2+) triggered epileptiform activity, which had decreased spike amplitude and prolonged interburst interval during application of the Px1 hemichannel blocking peptide. We conclude that Px1 hemichannel opening is triggered by NMDAR stimulation and can contribute to epileptiform seizure activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Roger J -- Jackson, Michael F -- Olah, Michelle E -- Rungta, Ravi L -- Hines, Dustin J -- Beazely, Michael A -- MacDonald, John F -- MacVicar, Brian A -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1555-9. doi: 10.1126/science.1165209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Brain Research Centre, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada. rj.thompson@ucalgary.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056988" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Calcium/metabolism ; Cells, Cultured ; Connexins/genetics/*physiology ; Dendrites/physiology ; Electrical Synapses/physiology ; Epilepsy/physiopathology ; Hippocampus/*physiology/physiopathology ; In Vitro Techniques ; Mice ; Nerve Tissue Proteins/genetics/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; RNA Interference ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synaptic Transmission
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  • 55
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    The spread of Ras activity triggered by activation of a single dendritic spine (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-17
    Description: In neurons, individual dendritic spines isolate N-methyl-d-aspartate (NMDA) receptor-mediated calcium ion (Ca2+) accumulations from the dendrite and other spines. However, the extent to which spines compartmentalize signaling events downstream of Ca2+ influx is not known. We combined two-photon fluorescence lifetime imaging with two-photon glutamate uncaging to image the activity of the small guanosine triphosphatase Ras after NMDA receptor activation at individual spines. Induction of long-term potentiation (LTP) triggered robust Ca2+-dependent Ras activation in single spines that decayed in approximately 5 minutes. Ras activity spread over approximately 10 micrometers of dendrite and invaded neighboring spines by diffusion. The spread of Ras-dependent signaling was necessary for the local regulation of the threshold for LTP induction. Thus, Ca2+-dependent synaptic signals can spread to couple multiple synapses on short stretches of dendrite.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745709/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harvey, Christopher D -- Yasuda, Ryohei -- Zhong, Haining -- Svoboda, Karel -- AS1398/Autism Speaks/ -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 MH080047-01/MH/NIMH NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Jul 4;321(5885):136-40. doi: 10.1126/science.1159675. Epub 2008 Jun 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Janelia Farm Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18556515" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Cell Membrane/metabolism ; Dendritic Spines/*physiology ; Diffusion ; Fluorescence Resonance Energy Transfer ; GTPase-Activating Proteins/metabolism ; Glutamic Acid/metabolism ; Guanine Nucleotide Exchange Factors/metabolism ; Hippocampus/cytology/physiology ; *Long-Term Potentiation ; Pyramidal Cells/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Synapses/*physiology ; Transfection ; ras Proteins/*metabolism
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  • 56
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    Surface mobility of postsynaptic AMPARs tunes synaptic transmission (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-12
    Description: AMPA glutamate receptors (AMPARs) mediate fast excitatory synaptic transmission. Upon fast consecutive synaptic stimulation, transmission can be depressed. Recuperation from fast synaptic depression has been attributed solely to recovery of transmitter release and/or AMPAR desensitization. We show that AMPAR lateral diffusion, observed in both intact hippocampi and cultured neurons, allows fast exchange of desensitized receptors with naive functional ones within or near the postsynaptic density. Recovery from depression in the tens of millisecond time range can be explained in part by this fast receptor exchange. Preventing AMPAR surface movements through cross-linking, endogenous clustering, or calcium rise all slow recovery from depression. Physiological regulation of postsynaptic receptor mobility affects the fidelity of synaptic transmission by shaping the frequency dependence of synaptic responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715948/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2715948/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heine, Martin -- Groc, Laurent -- Frischknecht, Renato -- Beique, Jean-Claude -- Lounis, Brahim -- Rumbaugh, Gavin -- Huganir, Richard L -- Cognet, Laurent -- Choquet, Daniel -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):201-5. doi: 10.1126/science.1152089.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, UMR 5091, Universite Bordeaux, Bordeaux, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403705" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/metabolism ; Cells, Cultured ; Diffusion ; Excitatory Amino Acid Antagonists/pharmacology ; Excitatory Postsynaptic Potentials ; Fluorescence Recovery After Photobleaching ; Glutamic Acid/metabolism ; Hippocampus/cytology/*physiology ; Kynurenic Acid/pharmacology ; Neuronal Plasticity ; Neurons/physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Synapses/drug effects/*physiology ; *Synaptic Transmission/drug effects ; Transfection
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    Neuroscience. A protoplasmic kiss to remember (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korte, Martin -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1627-8. doi: 10.1126/science.1155748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoological Institute, Division of Cellular Neurobiology, TU Braunschweig, D-38106 Germany. m.korte@tu-bs.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18356512" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Dendritic Spines/*physiology/*ultrastructure ; Glutamic Acid/metabolism ; *Neuronal Plasticity ; *Protein Biosynthesis ; Pyramidal Cells/physiology/*ultrastructure ; Rats ; Receptor, trkB/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology/ultrastructure
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    Cathepsin K-dependent toll-like receptor 9 signaling revealed in experimental arthritis (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-02-02
    Description: Cathepsin K was originally identified as an osteoclast-specific lysosomal protease, the inhibitor of which has been considered might have therapeutic potential. We show that inhibition of cathepsin K could potently suppress autoimmune inflammation of the joints as well as osteoclastic bone resorption in autoimmune arthritis. Furthermore, cathepsin K-/- mice were resistant to experimental autoimmune encephalomyelitis. Pharmacological inhibition or targeted disruption of cathepsin K resulted in defective Toll-like receptor 9 signaling in dendritic cells in response to unmethylated CpG DNA, which in turn led to attenuated induction of T helper 17 cells, without affecting the antigen-presenting ability of dendritic cells. These results suggest that cathepsin K plays an important role in the immune system and may serve as a valid therapeutic target in autoimmune diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asagiri, Masataka -- Hirai, Toshitake -- Kunigami, Toshihiro -- Kamano, Shunya -- Gober, Hans-Jurgen -- Okamoto, Kazuo -- Nishikawa, Keizo -- Latz, Eicke -- Golenbock, Douglas T -- Aoki, Kazuhiro -- Ohya, Keiichi -- Imai, Yuuki -- Morishita, Yasuyuki -- Miyazono, Kohei -- Kato, Shigeaki -- Saftig, Paul -- Takayanagi, Hiroshi -- New York, N.Y. -- Science. 2008 Feb 1;319(5863):624-7. doi: 10.1126/science.1150110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Signaling, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8549, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18239127" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Arthritis, Experimental/drug therapy/*immunology/*metabolism ; Autoimmune Diseases/drug therapy/immunology/*metabolism ; Bone Resorption ; Cathepsin K ; Cathepsins/antagonists & inhibitors/deficiency/*metabolism ; Cytokines/metabolism ; DNA/immunology/metabolism ; Dendritic Cells/drug effects/immunology ; Dinucleoside Phosphates/immunology/metabolism ; Encephalomyelitis, Autoimmune, Experimental/immunology/metabolism ; Endosomes/metabolism ; Freund's Adjuvant/immunology ; Lymphocyte Activation/drug effects ; Male ; Mice ; Osteoporosis/drug therapy ; Protease Inhibitors/pharmacology ; Rats ; *Signal Transduction ; T-Lymphocytes/drug effects/enzymology/immunology ; Toll-Like Receptor 9/*metabolism
    Print ISSN: 0036-8075
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    The antidepressant fluoxetine restores plasticity in the adult visual cortex (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-04-19
    Description: We investigated whether fluoxetine, a widely prescribed medication for treatment of depression, restores neuronal plasticity in the adult visual system of the rat. We found that chronic administration of fluoxetine reinstates ocular dominance plasticity in adulthood and promotes the recovery of visual functions in adult amblyopic animals, as tested electrophysiologically and behaviorally. These effects were accompanied by reduced intracortical inhibition and increased expression of brain-derived neurotrophic factor in the visual cortex. Cortical administration of diazepam prevented the effects induced by fluoxetine, indicating that the reduction of intracortical inhibition promotes visual cortical plasticity in the adult. Our results suggest a potential clinical application for fluoxetine in amblyopia as well as new mechanisms for the therapeutic effects of antidepressants and for the pathophysiology of mood disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maya Vetencourt, Jose Fernando -- Sale, Alessandro -- Viegi, Alessandro -- Baroncelli, Laura -- De Pasquale, Roberto -- O'Leary, Olivia F -- Castren, Eero -- Maffei, Lamberto -- New York, N.Y. -- Science. 2008 Apr 18;320(5874):385-8. doi: 10.1126/science.1150516.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scuola Normale Superiore, Piazza dei Cavalieri, I-56100 Pisa, Italy. jf.maya@in.cnr.it〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18420937" target="_blank"〉PubMed〈/a〉
    Keywords: Amblyopia/drug therapy/physiopathology ; Animals ; Antidepressive Agents, Second-Generation/pharmacology ; Brain-Derived Neurotrophic Factor/metabolism ; Diazepam/pharmacology ; Dominance, Ocular/drug effects ; Evoked Potentials, Visual/drug effects ; Fluoxetine/administration & dosage/*pharmacology ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Neuronal Plasticity/*drug effects ; Rats ; Serotonin/physiology ; Serotonin Uptake Inhibitors/*pharmacology ; Synaptic Transmission/drug effects ; Visual Cortex/*drug effects/physiology ; gamma-Aminobutyric Acid/metabolism
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    Activation of aldehyde dehydrogenase-2 reduces ischemic damage to the heart (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: There is substantial interest in the development of drugs that limit the extent of ischemia-induced cardiac damage caused by myocardial infarction or by certain surgical procedures. Here, using an unbiased proteomic search, we identified mitochondrial aldehyde dehydrogenase 2 (ALDH2) as an enzyme whose activation correlates with reduced ischemic heart damage in rodent models. A high-throughput screen yielded a small-molecule activator of ALDH2 (Alda-1) that, when administered to rats before an ischemic event, reduced infarct size by 60%, most likely through its inhibitory effect on the formation of cytotoxic aldehydes. In vitro, Alda-1 was a particularly effective activator of ALDH2*2, an inactive mutant form of the enzyme that is found in 40% of East Asian populations. Thus, pharmacologic enhancement of ALDH2 activity may be useful for patients with wild-type or mutant ALDH2 who are subjected to cardiac ischemia, such as during coronary bypass surgery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741612/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2741612/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Che-Hong -- Budas, Grant R -- Churchill, Eric N -- Disatnik, Marie-Helene -- Hurley, Thomas D -- Mochly-Rosen, Daria -- AA11147/AA/NIAAA NIH HHS/ -- R01 AA011147/AA/NIAAA NIH HHS/ -- R01 AA011147-08/AA/NIAAA NIH HHS/ -- R01 AA011147-09/AA/NIAAA NIH HHS/ -- R01 AA011147-10/AA/NIAAA NIH HHS/ -- R01 AA011147-11/AA/NIAAA NIH HHS/ -- R01 AA011147-12/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1493-5. doi: 10.1126/science.1158554.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305-5174, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787169" target="_blank"〉PubMed〈/a〉
    Keywords: Aldehyde Dehydrogenase/antagonists & inhibitors/*metabolism ; Aldehydes/metabolism ; Amino Acid Sequence ; Animals ; Benzamides/*pharmacology ; Benzodioxoles/*pharmacology ; Cardiotonic Agents/*pharmacology ; Cyanamide/pharmacology ; Enzyme Activation ; Ethanol/pharmacology ; Ischemic Preconditioning, Myocardial ; Mitochondrial Proteins/agonists/antagonists & inhibitors/*metabolism ; Molecular Sequence Data ; Myocardial Infarction/enzymology/pathology/*prevention & control ; Myocardial Reperfusion Injury/*enzymology ; Myocardium/*enzymology/pathology ; Nitroglycerin/pharmacology ; Phosphorylation ; Protein Kinase C-epsilon/metabolism ; Proteomics ; Rats ; Rats, Wistar
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    Finite scale of spatial representation in the hippocampus (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-07-05
    Description: To determine how spatial scale is represented in the pyramidal cell population of the hippocampus, we recorded neural activity at multiple longitudinal levels of this brain area while rats ran back and forth on an 18-meter-long linear track. CA3 cells had well-defined place fields at all levels. The scale of representation increased almost linearly from 〈1 meter at the dorsal pole to approximately 10 meters at the ventral pole. The results suggest that the place-cell map includes the entire hippocampus and that environments are represented in the hippocampus at a topographically graded but finite continuum of scales.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kjelstrup, Kirsten Brun -- Solstad, Trygve -- Brun, Vegard Heimly -- Hafting, Torkel -- Leutgeb, Stefan -- Witter, Menno P -- Moser, Edvard I -- Moser, May-Britt -- New York, N.Y. -- Science. 2008 Jul 4;321(5885):140-3. doi: 10.1126/science.1157086.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kavli Institute for Systems Neuroscience and Centre for the Biology of Memory, Norwegian University of Science and Technology, 7489 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18599792" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Algorithms ; Animals ; Brain Mapping ; Electrodes, Implanted ; Hippocampus/cytology/*physiology ; Learning ; Linear Models ; Male ; Pyramidal Cells/*physiology ; Rats ; Rats, Long-Evans ; *Space Perception ; Spatial Behavior ; Theta Rhythm
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    Video-rate far-field optical nanoscopy dissects synaptic vesicle movement (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-02-23
    Description: We present video-rate (28 frames per second) far-field optical imaging with a focal spot size of 62 nanometers in living cells. Fluorescently labeled synaptic vesicles inside the axons of cultured neurons were recorded with stimulated emission depletion (STED) microscopy in a 2.5-micrometer by 1.8-micrometer field of view. By reducing the cross-sectional area of the focal spot by about a factor of 18 below the diffraction limit (260 nanometers), STED allowed us to map and describe the vesicle mobility within the highly confined space of synaptic boutons. Although restricted within boutons, the vesicle movement was substantially faster in nonbouton areas, consistent with the observation that a sizable vesicle pool continuously transits through the axons. Our study demonstrates the emerging ability of optical microscopy to investigate intracellular physiological processes on the nanoscale in real time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westphal, Volker -- Rizzoli, Silvio O -- Lauterbach, Marcel A -- Kamin, Dirk -- Jahn, Reinhard -- Hell, Stefan W -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):246-9. doi: 10.1126/science.1154228. Epub 2008 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of NanoBiophotonics, Max-Planck-Institute for Biophysical Chemistry, Gottingen 37077, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18292304" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Axons/physiology/*ultrastructure ; Cells, Cultured ; Fluorescent Dyes ; Hippocampus/physiology/ultrastructure ; Kinetics ; Microscopy, Fluorescence/*methods ; Movement ; *Nanotechnology ; Optics and Photonics ; Rats ; Synaptic Vesicles/*physiology/*ultrastructure ; Video Recording
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    Representation of geometric borders in the entorhinal cortex (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-12-20
    Description: We report the existence of an entorhinal cell type that fires when an animal is close to the borders of the proximal environment. The orientation-specific edge-apposing activity of these "border cells" is maintained when the environment is stretched and during testing in enclosures of different size and shape in different rooms. Border cells are relatively sparse, making up less than 10% of the local cell population, but can be found in all layers of the medial entorhinal cortex as well as the adjacent parasubiculum, often intermingled with head-direction cells and grid cells. Border cells may be instrumental in planning trajectories and anchoring grid fields and place fields to a geometric reference frame.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solstad, Trygve -- Boccara, Charlotte N -- Kropff, Emilio -- Moser, May-Britt -- Moser, Edvard I -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1865-8. doi: 10.1126/science.1166466.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Kavli Institute for Systems Neuroscience and Centre for the Biology of Memory, Norwegian University of Science and Technology, 7489 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19095945" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cues ; Electrophysiology ; Entorhinal Cortex/*cytology/*physiology ; Male ; Neurons/*physiology ; *Orientation ; Rats ; Rats, Long-Evans ; *Space Perception
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    High impulsivity predicts the switch to compulsive cocaine-taking (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-06-07
    Description: Both impulsivity and novelty-seeking have been suggested to be behavioral markers of the propensity to take addictive drugs. However, their relevance for the vulnerability to compulsively seek and take drugs, which is a hallmark feature of addiction, is unknown. We report here that, whereas high reactivity to novelty predicts the propensity to initiate cocaine self-administration, high impulsivity predicts the development of addiction-like behavior in rats, including persistent or compulsive drug-taking in the face of aversive outcomes. This study shows experimental evidence that a shift from impulsivity to compulsivity occurs during the development of addictive behavior, which provides insights into the genesis and neural mechanisms of drug addiction.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2478705/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2478705/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Belin, David -- Mar, Adam C -- Dalley, Jeffrey W -- Robbins, Trevor W -- Everitt, Barry J -- G0600196/Medical Research Council/United Kingdom -- G0600196(77608)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2008 Jun 6;320(5881):1352-5. doi: 10.1126/science.1158136.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Behavioural and Clinical Neuroscience Institute and Department of Experimental Psychology, University of Cambridge, Downing Street, Cambridge CB2 3EB, UK. bdb26@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18535246" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*psychology ; *Compulsive Behavior ; Exploratory Behavior ; *Impulsive Behavior ; Male ; Models, Animal ; Motor Activity ; Rats ; Self Administration
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    Activation of FOXO1 by Cdk1 in cycling cells and postmitotic neurons (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-22
    Description: Activation of cyclin-dependent kinase 1 (Cdk1) has been linked to cell death of postmitotic neurons in brain development and disease. We found that Cdk1 phosphorylated the transcription factor FOXO1 at Ser249 in vitro and in vivo. The phosphorylation of FOXO1 at Ser249 disrupted FOXO1 binding with 14-3-3 proteins and thereby promoted the nuclear accumulation of FOXO1 and stimulated FOXO1-dependent transcription, leading to cell death in neurons. In proliferating cells, Cdk1 induced FOXO1 Ser249 phosphorylation at the G2/M phase of the cell cycle, resulting in FOXO1-dependent expression of the mitotic regulator Polo-like kinase (Plk). These findings define a conserved signaling link between Cdk1 and FOXO1 that may have a key role in diverse biological processes, including the degeneration of postmitotic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yuan, Zengqiang -- Becker, Esther B E -- Merlo, Paola -- Yamada, Tomoko -- DiBacco, Sara -- Konishi, Yoshiyuki -- Schaefer, Erik M -- Bonni, Azad -- NS047188/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1665-8. doi: 10.1126/science.1152337.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18356527" target="_blank"〉PubMed〈/a〉
    Keywords: 14-3-3 Proteins/metabolism ; Animals ; Apoptosis ; CDC2 Protein Kinase/*metabolism ; *Cell Cycle ; Cell Cycle Proteins/genetics/metabolism ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Cell Proliferation ; Cells, Cultured ; Forkhead Transcription Factors/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Nerve Tissue Proteins/*metabolism ; Neurons/cytology/*metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases/genetics/metabolism ; Proto-Oncogene Proteins/genetics/metabolism ; Rats ; Serine/metabolism ; Signal Transduction ; Transcription, Genetic
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    Rule learning by rats (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-29
    Description: Using rules extracted from experience to solve problems in novel situations involves cognitions such as analogical reasoning and language learning and is considered a keystone of humans' unique abilities. Nonprimates, it has been argued, lack such rule transfer. We report that Rattus norvegicus can learn simple rules and apply them to new situations. Rats learned that sequences of stimuli consistent with a rule (such as XYX) were different from other sequences (such as XXY or YXX). When novel stimuli were used to construct sequences that did or did not obey the previously learned rule, rats transferred their learning. Therefore, rats, like humans, can transfer structural knowledge from sequential experiences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, Robin A -- Mondragon, Esther -- Murphy, Victoria A -- S20033/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1849-51. doi: 10.1126/science.1151564.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University College London, Gower Street, London WC1E 6BT, UK. robin.murphy@ucl.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cognition ; Cues ; *Learning ; Male ; Rats ; Reinforcement (Psychology) ; *Transfer (Psychology)
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    Spontaneous changes of neocortical code for associative memory during consolidation (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-08
    Description: After learning, the medial prefrontal cortex (mPFC) gradually comes to modulate the expression of memories that initially depended on the hippocampus. We show that during this consolidation period, neural firing in the mPFC becomes selective for the acquired memories. After acquisition of memory associations, neuron populations in the mPFC of rats developed sustained activity during the interval between two paired stimuli, but reduced activity during the corresponding interval between two unpaired stimuli. These new patterns developed over a period of several weeks after learning, with and without continued conditioning trials. Thus, in agreement with a central tenet of consolidation theory, acquired associations initiate subsequent, gradual processes that result in lasting changes of the mPFC's code, without continued training.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Takehara-Nishiuchi, Kaori -- McNaughton, Bruce L -- MH046823/MH/NIMH NIH HHS/ -- NS020331/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):960-3. doi: 10.1126/science.1161299.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arizona Research Laboratories, Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson, AZ 85724-5115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Association Learning/*physiology ; Blinking ; Conditioning (Psychology) ; Electrodes, Implanted ; Hippocampus/physiology ; Male ; Memory/*physiology ; Neocortex/*physiology ; Neurons/physiology ; Prefrontal Cortex/*physiology ; Rats
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    Muscular thin films for building actuators and powering devices (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-08
    Description: We demonstrate the assembly of biohybrid materials from engineered tissues and synthetic polymer thin films. The constructs were built by culturing neonatal rat ventricular cardiomyocytes on polydimethylsiloxane thin films micropatterned with extracellular matrix proteins to promote spatially ordered, two-dimensional myogenesis. The constructs, termed muscular thin films, adopted functional, three-dimensional conformations when released from a thermally sensitive polymer substrate and were designed to perform biomimetic tasks by varying tissue architecture, thin-film shape, and electrical-pacing protocol. These centimeter-scale constructs perform functions as diverse as gripping, pumping, walking, and swimming with fine spatial and temporal control and generating specific forces as high as 4 millinewtons per square millimeter.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Feinberg, Adam W -- Feigel, Alex -- Shevkoplyas, Sergey S -- Sheehy, Sean -- Whitesides, George M -- Parker, Kevin Kit -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1366-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Disease Biophysics Group, School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17823347" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anisotropy ; Cell Culture Techniques ; Cells, Cultured ; Dimethylpolysiloxanes ; Microscopy, Fluorescence ; Motion ; Muscle Contraction ; *Myocardium ; Myocytes, Cardiac ; Rats ; Rats, Sprague-Dawley ; Robotics ; Silicones ; *Tissue Engineering
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    Structure of Nup58/45 suggests flexible nuclear pore diameter by intermolecular sliding (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-03-24
    Description: The nucleoporins Nup58 and Nup45 are part of the central transport channel of the nuclear pore complex, which is thought to have a flexible diameter. In the crystal structure of an alpha-helical region of mammalian Nup58/45, we identified distinct tetramers, each consisting of two antiparallel hairpin dimers. The intradimeric interface is hydrophobic, whereas dimer-dimer association occurs through large hydrophilic residues. These residues are laterally displaced in various tetramer conformations, which suggests an intermolecular sliding by 11 angstroms. We propose that circumferential sliding plays a role in adjusting the diameter of the central transport channel.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Melcak, Ivo -- Hoelz, Andre -- Blobel, Gunter -- R01 GM111461/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1729-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell Biology, Howard Hughes Medical Institute, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379812" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Crystallization ; Crystallography, X-Ray ; Dimerization ; Hydrogen Bonding ; Hydrophobic and Hydrophilic Interactions ; Membrane Glycoproteins/chemistry ; Molecular Sequence Data ; Nuclear Pore Complex Proteins/*chemistry ; Protein Folding ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Rats ; Static Electricity
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Anatomy and dynamics of a supramolecular membrane protein cluster (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: Most plasmalemmal proteins organize in submicrometer-sized clusters whose architecture and dynamics are still enigmatic. With syntaxin 1 as an example, we applied a combination of far-field optical nanoscopy, biochemistry, fluorescence recovery after photobleaching (FRAP) analysis, and simulations to show that clustering can be explained by self-organization based on simple physical principles. On average, the syntaxin clusters exhibit a diameter of 50 to 60 nanometers and contain 75 densely crowded syntaxins that dynamically exchange with freely diffusing molecules. Self-association depends on weak homophilic protein-protein interactions. Simulations suggest that clustering immobilizes and conformationally constrains the molecules. Moreover, a balance between self-association and crowding-induced steric repulsions is sufficient to explain both the size and dynamics of syntaxin clusters and likely of many oligomerizing membrane proteins that form supramolecular structures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sieber, Jochen J -- Willig, Katrin I -- Kutzner, Carsten -- Gerding-Reimers, Claas -- Harke, Benjamin -- Donnert, Gerald -- Rammner, Burkhard -- Eggeling, Christian -- Hell, Stefan W -- Grubmuller, Helmut -- Lang, Thorsten -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1072-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717182" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cell Membrane/chemistry/*metabolism ; Chemistry, Physical ; Computer Simulation ; Diffusion ; Fluorescence Recovery After Photobleaching ; Green Fluorescent Proteins ; Immunoblotting ; Microscopy, Confocal ; Microscopy, Fluorescence ; Models, Biological ; Nanotechnology ; PC12 Cells ; Physicochemical Phenomena ; Protein Structure, Tertiary ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Syntaxin 1/*chemistry/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hardwiring the brain: endocannabinoids shape neuronal connectivity (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-26
    Description: The roles of endocannabinoid signaling during central nervous system development are unknown. We report that CB(1) cannabinoid receptors (CB(1)Rs) are enriched in the axonal growth cones of gamma-aminobutyric acid-containing (GABAergic) interneurons in the rodent cortex during late gestation. Endocannabinoids trigger CB(1)R internalization and elimination from filopodia and induce chemorepulsion and collapse of axonal growth cones of these GABAergic interneurons by activating RhoA. Similarly, endocannabinoids diminish the galvanotropism of Xenopus laevis spinal neurons. These findings, together with the impaired target selection of cortical GABAergic interneurons lacking CB(1)Rs, identify endocannabinoids as axon guidance cues and demonstrate that endocannabinoid signaling regulates synaptogenesis and target selection in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berghuis, Paul -- Rajnicek, Ann M -- Morozov, Yury M -- Ross, Ruth A -- Mulder, Jan -- Urban, Gabriella M -- Monory, Krisztina -- Marsicano, Giovanni -- Matteoli, Michela -- Canty, Alison -- Irving, Andrew J -- Katona, Istvan -- Yanagawa, Yuchio -- Rakic, Pasko -- Lutz, Beat -- Mackie, Ken -- Harkany, Tibor -- DA00286/DA/NIDA NIH HHS/ -- DA015916/DA/NIDA NIH HHS/ -- DA11322/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 2007 May 25;316(5828):1212-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, S-17177 Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17525344" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cannabinoid Receptor Modulators/metabolism/*physiology ; Cell Movement ; Cells, Cultured ; Cerebral Cortex/cytology/embryology/ultrastructure ; *Endocannabinoids ; Growth Cones/physiology/ultrasonography ; In Situ Hybridization ; Interneurons/metabolism/*physiology/ultrasonography ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Rats ; Rats, Sprague-Dawley ; Receptor, Cannabinoid, CB1/agonists/*physiology ; Signal Transduction ; Stem Cells/metabolism ; Synapses/physiology/ultrasonography ; Xenopus Proteins/physiology ; Xenopus laevis ; gamma-Aminobutyric Acid/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Anti-Hebbian long-term potentiation in the hippocampal feedback inhibitory circuit (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: Long-term potentiation (LTP), which approximates Hebb's postulate of associative learning, typically requires depolarization-dependent glutamate receptors of the NMDA (N-methyl-D-aspartate) subtype. However, in some neurons, LTP depends instead on calcium-permeable AMPA-type receptors. This is paradoxical because intracellular polyamines block such receptors during depolarization. We report that LTP at synapses on hippocampal interneurons mediating feedback inhibition is "anti-Hebbian":Itis induced by presynaptic activity but prevented by postsynaptic depolarization. Anti-Hebbian LTP may occur in interneurons that are silent during periods of intense pyramidal cell firing, such as sharp waves, and lead to their altered activation during theta activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369266/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3369266/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamsa, Karri P -- Heeroma, Joost H -- Somogyi, Peter -- Rusakov, Dmitri A -- Kullmann, Dimitri M -- 071179/Wellcome Trust/United Kingdom -- G0400627/Medical Research Council/United Kingdom -- G0400627(71256)/Medical Research Council/United Kingdom -- G0400627(76527)/Medical Research Council/United Kingdom -- G0501424/Medical Research Council/United Kingdom -- G0600368/Medical Research Council/United Kingdom -- G0600368(77987)/Medical Research Council/United Kingdom -- MC_U138135973/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1262-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Neurology, University College London, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332410" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology/*physiology ; Interneurons/*physiology ; *Long-Term Potentiation ; Male ; Membrane Potentials ; Neural Inhibition/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Spermine/analogs & derivatives/pharmacology ; Synapses/*physiology
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    Neuroscience. Rapid consolidation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-04-07
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2271071/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2271071/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Squire, Larry R -- R01 MH024600/MH/NIMH NIH HHS/ -- R01 MH024600-33/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2007 Apr 6;316(5821):57-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉VA Medical Center, San Diego, CA 92161, USA. lsquire@ucsd.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412942" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Association Learning ; Cues ; Hippocampus/*physiology ; *Memory ; Mental Recall ; Neocortex/*physiology ; Rats ; Time Factors
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    Neuroscience. Spying on new neurons in the human brain (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):899-900.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991833" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Adult Stem Cells/chemistry/*cytology ; Animals ; Biomarkers/*analysis ; Brain/cytology/embryology ; Brain Chemistry ; Child ; Fatty Acids/analysis ; Hippocampus/chemistry/*cytology ; Humans ; Magnetic Resonance Spectroscopy/*methods ; Mice ; Rats ; Stem Cells/chemistry/*cytology
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    Inactivation of the interoceptive insula disrupts drug craving and malaise induced by lithium (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-10-27
    Description: Addiction profoundly alters motivational circuits so that drugs become powerful reinforcers of behavior. The interoceptive system continuously updates homeostatic and emotional information that are important elements in motivational decisions. We tested the idea that interoceptive information is essential in drug craving and in the behavioral signs of malaise. We inactivated the primary interoceptive cortex in amphetamine-experienced rats, which prevented the urge to seek amphetamine in a place preference task. Interoceptive insula inactivation also blunted the signs of malaise induced by acute lithium administration. Drug-seeking and malaise both induced Fos expression, a marker of neuronal activation, in the insula. We conclude that the insular cortex is a key structure in the perception of bodily needs that provides direction to motivated behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Contreras, Marco -- Ceric, Francisco -- Torrealba, Fernando -- New York, N.Y. -- Science. 2007 Oct 26;318(5850):655-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departamento de Fisiologia, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile, Santiago 6513677, Chile.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17962567" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine-Related Disorders/*physiopathology ; Animals ; *Behavior, Addictive ; *Behavior, Animal/drug effects ; Cerebral Cortex/*physiology/physiopathology ; Conditioning (Psychology) ; Dextroamphetamine/administration & dosage ; Fatigue/*chemically induced ; Lidocaine/administration & dosage/pharmacology ; Lithium Chloride/administration & dosage/*pharmacology ; Male ; Motor Activity/*drug effects ; Rats
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    Temporal frequency of subthreshold oscillations scales with entorhinal grid cell field spacing (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-24
    Description: Grid cells in layer II of rat entorhinal cortex fire to spatial locations in a repeating hexagonal grid, with smaller spacing between grid fields for neurons in more dorsal anatomical locations. Data from in vitro whole-cell patch recordings showed differences in frequency of subthreshold membrane potential oscillations in entorhinal neurons that correspond to different positions along the dorsal-to-ventral axis, supporting a model of physiological mechanisms for grid cell responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950607/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950607/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giocomo, Lisa M -- Zilli, Eric A -- Fransen, Erik -- Hasselmo, Michael E -- DA16454/DA/NIDA NIH HHS/ -- MH60013/MH/NIMH NIH HHS/ -- MH71702/MH/NIMH NIH HHS/ -- P50 MH071702/MH/NIMH NIH HHS/ -- P50 MH071702-01A20004/MH/NIMH NIH HHS/ -- R01 DA016454/DA/NIDA NIH HHS/ -- R01 DA016454-04/DA/NIDA NIH HHS/ -- R01 DA016454-05/DA/NIDA NIH HHS/ -- R01 MH060013/MH/NIMH NIH HHS/ -- R01 MH060013-05/MH/NIMH NIH HHS/ -- R01 MH060013-06/MH/NIMH NIH HHS/ -- R01 MH061492/MH/NIMH NIH HHS/ -- R01 MH061492-05/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2007 Mar 23;315(5819):1719-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Memory and Brain, Department of Psychology, Program in Neuroscience, Boston University, 2 Cummington Street, Boston, MA 02215, USA. giocomo@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17379810" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Computer Simulation ; Dendrites/physiology ; Electric Stimulation ; Entorhinal Cortex/*cytology/*physiology ; Female ; In Vitro Techniques ; Male ; Mathematics ; Membrane Potentials ; Models, Neurological ; Movement ; Neurons/cytology/*physiology ; Patch-Clamp Techniques ; Periodicity ; Rats ; Rats, Long-Evans ; Space Perception ; Time Factors
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    Cancer research. Probing the roots of race and cancer (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Couzin, Jennifer -- New York, N.Y. -- Science. 2007 Feb 2;315(5812):592-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17272699" target="_blank"〉PubMed〈/a〉
    Keywords: Africa/epidemiology ; *African Americans/genetics/statistics & numerical data ; African Continental Ancestry Group/genetics/statistics & numerical data ; Animals ; Breast Neoplasms/*ethnology/genetics/mortality/physiopathology ; DNA Methylation ; Environment ; Female ; Health Services Accessibility ; Humans ; Rats ; Social Isolation ; Stress, Physiological/physiopathology ; United States/epidemiology
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    Medicine. The yin-yang of sirtuins (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dillin, Andrew -- Kelly, Jeffery W -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):461-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA. dillin@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17656709" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Autophagy ; Cell Line, Tumor ; Disease Models, Animal ; Drosophila melanogaster ; Humans ; Neurodegenerative Diseases/physiopathology ; Parkinson Disease/drug therapy/pathology/*physiopathology ; RNA Interference ; Rats ; Signal Transduction ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/genetics/metabolism/*physiology ; Transfection ; alpha-Synuclein/metabolism
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    High-speed imaging reveals neurophysiological links to behavior in an animal model of depression (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-07-07
    Description: The hippocampus is one of several brain areas thought to play a central role in affective behaviors, but the underlying local network dynamics are not understood. We used quantitative voltage-sensitive dye imaging to probe hippocampal dynamics with millisecond resolution in brain slices after bidirectional modulation of affective state in rat models of depression. We found that a simple measure of real-time activity-stimulus-evoked percolation of activity through the dentate gyrus relative to the hippocampal output subfield-accounted for induced changes in animal behavior independent of the underlying mechanism of action of the treatments. Our results define a circuit-level neurophysiological endophenotype for affective behavior and suggest an approach to understanding circuit-level substrates underlying psychiatric disease symptoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Airan, Raag D -- Meltzer, Leslie A -- Roy, Madhuri -- Gong, Yuqing -- Chen, Han -- Deisseroth, Karl -- New York, N.Y. -- Science. 2007 Aug 10;317(5839):819-23. Epub 2007 Jul 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioengineering, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17615305" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidepressive Agents, Tricyclic/pharmacology ; Behavior, Animal/drug effects ; Dentate Gyrus/pathology/*physiopathology ; Depressive Disorder/pathology/*physiopathology ; Diagnostic Imaging ; Disease Models, Animal ; Electric Stimulation ; Electrophysiology ; Female ; Fluoxetine/pharmacology ; Hippocampus/pathology/*physiopathology ; Imipramine/pharmacology ; Motor Activity/drug effects ; Nerve Net/*physiopathology ; Neurons/cytology/physiology ; Rats ; Rats, Inbred F344 ; Serotonin Uptake Inhibitors/pharmacology ; Stress, Physiological/physiopathology
    Print ISSN: 0036-8075
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    Cysteine redox sensor in PKGIa enables oxidant-induced activation (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Changes in the concentration of oxidants in cells can regulate biochemical signaling mechanisms that control cell function. We have found that guanosine 3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) functions directly as a redox sensor. The Ialpha isoform, PKGIalpha, formed an interprotein disulfide linking its two subunits in cells exposed to exogenous hydrogen peroxide. This oxidation directly activated the kinase in vitro, and in rat cells and tissues. The affinity of the kinase for substrates it phosphorylates was enhanced by disulfide formation. This oxidation-induced activation represents an alternate mechanism for regulation along with the classical activation involving nitric oxide and cGMP. This mechanism underlies cGMP-independent vasorelaxation in response to oxidants in the cardiovascular system and provides a molecular explantion for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burgoyne, Joseph R -- Madhani, Melanie -- Cuello, Friederike -- Charles, Rebecca L -- Brennan, Jonathan P -- Schroder, Ewald -- Browning, Darren D -- Eaton, Philip -- G0700320/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Sep 7;317(5843):1393-7. Epub 2007 Aug 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cardiology, Cardiovascular Division, King's College London, Rayne Institute, St. Thomas' Hospital, London SE1 7EH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Cell Line ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/genetics/*metabolism ; Cysteine/*metabolism ; Disulfides/metabolism ; Enzyme Activation ; Humans ; Hydrogen Peroxide/metabolism ; Male ; Nitric Oxide/metabolism ; Oxidants/*metabolism ; Oxidation-Reduction ; Oxidative Stress ; Rats ; Rats, Wistar ; Signal Transduction ; Tissue Culture Techniques ; Transfection ; Vasodilation/physiology
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    Schemas and memory consolidation (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Memory encoding occurs rapidly, but the consolidation of memory in the neocortex has long been held to be a more gradual process. We now report, however, that systems consolidation can occur extremely quickly if an associative "schema" into which new information is incorporated has previously been created. In experiments using a hippocampal-dependent paired-associate task for rats, the memory of flavor-place associations became persistent over time as a putative neocortical schema gradually developed. New traces, trained for only one trial, then became assimilated and rapidly hippocampal-independent. Schemas also played a causal role in the creation of lasting associative memory representations during one-trial learning. The concept of neocortical schemas may unite psychological accounts of knowledge structures with neurobiological theories of systems memory consolidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tse, Dorothy -- Langston, Rosamund F -- Kakeyama, Masaki -- Bethus, Ingrid -- Spooner, Patrick A -- Wood, Emma R -- Witter, Menno P -- Morris, Richard G M -- G9200370/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 6;316(5821):76-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cognitive Neuroscience, Centre for Cognitive and Neural Systems, and Centre for Neuroscience Research, University of Edinburgh, 1 George Square, Edinburgh EH8 9JZ, Scotland, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412951" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Association Learning ; Cues ; Hippocampus/*physiology ; Male ; *Memory ; Mental Recall ; Neocortex/*physiology ; Rats ; Time Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    An ATP gate controls tubulin binding by the tethered head of kinesin-1 (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-07
    Description: Kinesin-1 is a two-headed molecular motor that walks along microtubules, with each step gated by adenosine triphosphate (ATP) binding. Existing models for the gating mechanism propose a role for the microtubule lattice. We show that unpolymerized tubulin binds to kinesin-1, causing tubulin-activated release of adenosine diphosphate (ADP). With no added nucleotide, each kinesin-1 dimer binds one tubulin heterodimer. In adenylyl-imidodiphosphate (AMP-PNP), a nonhydrolyzable ATP analog, each kinesin-1 dimer binds two tubulin heterodimers. The data reveal an ATP gate that operates independently of the microtubule lattice, by ATP-dependent release of a steric or allosteric block on the tubulin binding site of the tethered kinesin-ADP head.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2504013/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2504013/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonso, Maria C -- Drummond, Douglas R -- Kain, Susan -- Hoeng, Julia -- Amos, Linda -- Cross, Robert A -- G0200542/Medical Research Council/United Kingdom -- G0200542(63814)/Medical Research Council/United Kingdom -- MC_U105184313/Medical Research Council/United Kingdom -- U.1051.04.002(78842)/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 6;316(5821):120-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Motors Group, Marie Curie Research Institute, The Chart, Oxted, Surrey RH8 0TL, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17412962" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/*metabolism ; Adenylyl Imidodiphosphate/metabolism ; Animals ; Binding Sites ; Dimerization ; Kinesin/chemistry/*metabolism ; Microtubules/*metabolism ; Models, Biological ; Molecular Motor Proteins/*metabolism ; Neurospora ; Protein Conformation ; Rats ; Recombinant Fusion Proteins/chemistry/metabolism ; Schizosaccharomyces ; Tubulin/chemistry/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 83
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    A MicroRNA feedback circuit in midbrain dopamine neurons (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-01
    Description: MicroRNAs (miRNAs) are evolutionarily conserved, 18- to 25-nucleotide, non-protein coding transcripts that posttranscriptionally regulate gene expression during development. miRNAs also occur in postmitotic cells, such as neurons in the mammalian central nervous system, but their function is less well characterized. We investigated the role of miRNAs in mammalian midbrain dopaminergic neurons (DNs). We identified a miRNA, miR-133b, that is specifically expressed in midbrain DNs and is deficient in midbrain tissue from patients with Parkinson's disease. miR-133b regulates the maturation and function of midbrain DNs within a negative feedback circuit that includes the paired-like homeodomain transcription factor Pitx3. We propose a role for this feedback circuit in the fine-tuning of dopaminergic behaviors such as locomotion.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2782470/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jongpil -- Inoue, Keiichi -- Ishii, Jennifer -- Vanti, William B -- Voronov, Sergey V -- Murchison, Elizabeth -- Hannon, Gregory -- Abeliovich, Asa -- R01 NS064433/NS/NINDS NIH HHS/ -- R01 NS064433-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 31;317(5842):1220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Neurology, Center for Neurobiology and Behavior, and Taub Institute, Columbia University, College of Physicians and Surgeons 15-403, 630 West 168th Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17761882" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cell Differentiation ; Cell Line ; Cells, Cultured ; Dopamine/*metabolism ; Embryonic Stem Cells ; *Feedback, Physiological ; Female ; Gene Expression Regulation ; Homeodomain Proteins/*metabolism ; Humans ; Locomotion ; Male ; Mesencephalon/cytology/*metabolism ; Mice ; MicroRNAs/*metabolism ; Middle Aged ; Models, Biological ; Neurons/cytology/*metabolism ; Parkinson Disease/metabolism ; Rats ; Ribonuclease III/genetics/metabolism ; Transcription Factors/*metabolism ; Transcription, Genetic
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  • 84
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    Comment on "Maternal oxytocin triggers a transient inhibitory switch in GABA signaling in the fetal brain during delivery" (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: Tyzio et al. (Reports, 15 December 2006, p. 1788) reported that maternal oxytocin triggers a transient excitatory-to-inhibitory switch of gamma-aminobutyric acid (GABA) signaling during labor, thus protecting the fetal rat brain from anoxic injury. However, a body of evidence supports the possibility that oxytocin is released from the fetal pituitary during delivery, not only from the mother, particularly under conditions of hypoxic stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carbillon, Lionel -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):197; author reply 197.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, Assistance Publique-Hopitaux de Paris, Paris 13 University, Hopital Jean Verdier, Avenue du 14 Juillet, 93143 Bondy Cedex, France. lionel.carbillon@jvr.aphp.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Brain/*embryology/metabolism ; Female ; Fetal Hypoxia/physiopathology/prevention & control ; Fetus/*metabolism ; Hippocampus/embryology/metabolism ; Oxytocin/metabolism/*physiology ; *Parturition ; Pituitary Gland/embryology/metabolism ; Pregnancy ; Rats ; *Signal Transduction ; gamma-Aminobutyric Acid/*metabolism
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    Promotion of tissue inflammation by the immune receptor Tim-3 expressed on innate immune cells (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-17
    Description: CD4+ T helper 1 (TH1) cells are important mediators of inflammation and are regulated by numerous pathways, including the negative immune receptor Tim-3. We found that Tim-3 is constitutively expressed on cells of the innate immune system in both mice and humans, and that it can synergize with Toll-like receptors. Moreover, an antibody agonist of Tim-3 acted as an adjuvant during induced immune responses, and Tim-3 ligation induced distinct signaling events in T cells and dendritic cells; the latter finding could explain the apparent divergent functions of Tim-3 in these cell types. Thus, by virtue of differential expression on innate versus adaptive immune cells, Tim-3 can either promote or terminate TH1 immunity and may be able to influence a range of inflammatory conditions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Ana C -- Anderson, David E -- Bregoli, Lisa -- Hastings, William D -- Kassam, Nasim -- Lei, Charles -- Chandwaskar, Rucha -- Karman, Jozsef -- Su, Ee W -- Hirashima, Mitsuomi -- Bruce, Jeffrey N -- Kane, Lawrence P -- Kuchroo, Vijay K -- Hafler, David A -- R01 AI067544/AI/NIAID NIH HHS/ -- R01 AI067544-01A2/AI/NIAID NIH HHS/ -- R56 AI067544/AI/NIAID NIH HHS/ -- R56 AI067544-01A1/AI/NIAID NIH HHS/ -- R56 AI067544-02/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1141-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD11b/immunology ; Astrocytes/immunology ; Central Nervous System Neoplasms/immunology ; Dendritic Cells/immunology ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Galectins/immunology ; Glioblastoma/immunology ; Humans ; Immunity, Innate ; Inflammation Mediators/*immunology ; Lipopolysaccharides/immunology ; Macrophages/immunology ; Membrane Proteins/biosynthesis/*immunology ; Mice ; Microglia/immunology ; Multiple Sclerosis/immunology ; Rats ; Receptors, Immunologic/biosynthesis/*immunology ; Receptors, Virus/biosynthesis/*immunology ; Signal Transduction ; T-Lymphocytes/immunology ; Th1 Cells/*immunology ; Toll-Like Receptors
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  • 86
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    Fast-forward playback of recent memory sequences in prefrontal cortex during sleep (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-11-17
    Description: As previously shown in the hippocampus and other brain areas, patterns of firing-rate correlations between neurons in the rat medial prefrontal cortex during a repetitive sequence task were preserved during subsequent sleep, suggesting that waking patterns are reactivated. We found that, during sleep, reactivation of spatiotemporal patterns was coherent across the network and compressed in time by a factor of 6 to 7. Thus, when behavioral constraints are removed, the brain's intrinsic processing speed may be much faster than it is in real time. Given recent evidence implicating the medial prefrontal cortex in retrieval of long-term memories, the observed replay may play a role in the process of memory consolidation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Euston, David R -- Tatsuno, Masami -- McNaughton, Bruce L -- MH046823/MH/NIMH NIH HHS/ -- NS020331/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 16;318(5853):1147-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arizona Research Laboratories Division of Neural Systems, Memory and Aging, University of Arizona, Tucson, AZ 85724-5115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18006749" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Hippocampus/physiology ; Male ; Memory/*physiology ; Prefrontal Cortex/*physiology ; Rats ; Rats, Inbred F344 ; Reaction Time ; Sleep/*physiology
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  • 87
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    Rapid erasure of long-term memory associations in the cortex by an inhibitor of PKM zeta (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-19
    Description: Little is known about the neuronal mechanisms that subserve long-term memory persistence in the brain. The components of the remodeled synaptic machinery, and how they sustain the new synaptic or cellwide configuration over time, are yet to be elucidated. In the rat cortex, long-term associative memories vanished rapidly after local application of an inhibitor of the protein kinase C isoform, protein kinase M zeta (PKMzeta). The effect was observed for at least several weeks after encoding and may be irreversible. In the neocortex, which is assumed to be the repository of multiple types of long-term memory, persistence of memory is thus dependent on ongoing activity of a protein kinase long after that memory is considered to have consolidated into a long-term stable form.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shema, Reut -- Sacktor, Todd Charlton -- Dudai, Yadin -- MH57068/MH/NIMH NIH HHS/ -- R01 MH53576/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):951-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Weizmann Institute of Science, Rehovot 76100, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702943" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Enzyme Inhibitors/administration & dosage/*pharmacology ; Hippocampus/drug effects/enzymology/physiology ; Male ; Memory/*drug effects/*physiology ; Neocortex/drug effects/enzymology/*physiology ; Oligopeptides/administration & dosage/*pharmacology ; Protein Kinase C/*antagonists & inhibitors/*metabolism ; Rats ; Rats, Wistar ; Taste ; Time Factors
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    Neuroscience. Where am I? (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-02-17
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fenton, Andre A -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):947-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Pharmacology, Robert F. Furchgott Center for Neural and Behavioral Science, State University of New York Downstate Medical Center, Brooklyn, NY 11203, USA. afenton@downstate.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303741" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dentate Gyrus/physiology ; Hippocampus/*physiology ; Humans ; Neurons/physiology ; Orientation/*physiology ; Rats ; Space Perception/*physiology
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  • 89
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    Requirement of inositol pyrophosphates for full exocytotic capacity in pancreatic beta cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-24
    Description: Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic beta cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in beta cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic beta cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Illies, Christopher -- Gromada, Jesper -- Fiume, Roberta -- Leibiger, Barbara -- Yu, Jia -- Juhl, Kirstine -- Yang, Shao-Nian -- Barma, Deb K -- Falck, John R -- Saiardi, Adolfo -- Barker, Christopher J -- Berggren, Per-Olof -- GM31278/GM/NIGMS NIH HHS/ -- MC_U122680443/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Nov 23;318(5854):1299-302.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, SE-171 76, Stockholm, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18033884" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cricetinae ; Electric Capacitance ; *Exocytosis ; Inositol Phosphates/*metabolism ; Insulin/*secretion ; Insulin-Secreting Cells/*metabolism/secretion ; Islets of Langerhans/metabolism ; Mice ; Patch-Clamp Techniques ; Phosphotransferases (Phosphate Group Acceptor)/genetics/metabolism ; Phytic Acid/metabolism ; RNA Interference ; Rats ; Secretory Vesicles/*metabolism ; Transfection
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  • 90
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    Neuroscience. Shining light on depression (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-11
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993542/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993542/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Insel, Thomas R -- Z99 MH999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2007 Aug 10;317(5839):757-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute for Mental Health, Bethesda, MD 20892, USA. tinsel@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17690279" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coloring Agents ; Depressive Disorder/pathology/*physiopathology ; *Diagnostic Imaging ; Disease Models, Animal ; Gyrus Cinguli/pathology/*physiopathology ; Hippocampus/pathology/*physiopathology ; Humans ; Nerve Net/physiopathology ; Prefrontal Cortex/pathology/*physiopathology ; Rats
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    Biochemistry. Crowds of syntaxins (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, Stephen H -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1045-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, University of California at Irvine, Irvine, CA 92697, USA. stephen.white@uci.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717175" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Animals ; Cell Membrane/chemistry/*metabolism ; Computer Simulation ; Diffusion ; Exocytosis ; Fluorescence Recovery After Photobleaching ; Immunoblotting ; Microscopy, Confocal ; Microscopy, Fluorescence ; Models, Biological ; PC12 Cells ; Protein Structure, Tertiary ; Rats ; Secretory Vesicles/metabolism ; Syntaxin 1/*chemistry/*metabolism
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  • 92
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    Astrocytes potentiate transmitter release at single hippocampal synapses (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-25
    Description: Astrocytes play active roles in brain physiology. They respond to neurotransmitters and modulate neuronal excitability and synaptic function. However, the influence of astrocytes on synaptic transmission and plasticity at the single synapse level is unknown. Ca(2+) elevation in astrocytes transiently increased the probability of transmitter release at hippocampal area CA3-CA1 synapses, without affecting the amplitude of synaptic events. This form of short-term plasticity was due to the release of glutamate from astrocytes, a process that depended on Ca(2+) and soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein and that activated metabotropic glutamate receptors (mGluRs). The transient potentiation of transmitter release became persistent when the astrocytic signal was temporally coincident with postsynaptic depolarization. This persistent plasticity was mGluR-mediated but N-methyl-d-aspartate receptor-independent. These results indicate that astrocytes are actively involved in the transfer and storage of synaptic information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perea, Gertrudis -- Araque, Alfonso -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1083-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto Cajal, Consejo Superior de Investigaciones Cientificas, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717185" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Astrocytes/*physiology ; Calcium/metabolism ; Calcium Signaling ; Excitatory Postsynaptic Potentials ; Glutamic Acid/metabolism ; Hippocampus/*cytology/physiology ; Long-Term Potentiation ; Neuronal Plasticity ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, Metabotropic Glutamate/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; *Synaptic Transmission
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    Neuroscience. Enzyme keeps old memories alive (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-08-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2007 Aug 17;317(5840):883.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17702916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Cortex/drug effects/enzymology/physiology ; Enzyme Inhibitors/pharmacology ; Hippocampus/drug effects/enzymology ; Long-Term Potentiation/drug effects ; Memory/drug effects/*physiology ; Protein Kinase C/antagonists & inhibitors/*metabolism ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Trait or state? (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-08-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crabbe, John C -- Cunningham, Christopher L -- New York, N.Y. -- Science. 2007 Aug 24;317(5841):1033-5; author reply 1033-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17717168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/*administration & dosage ; Genotype ; *Impulsive Behavior/genetics ; Mice ; Nucleus Accumbens/metabolism ; Rats ; Receptors, Dopamine D2/metabolism ; Receptors, Dopamine D3/metabolism ; Self Administration
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Pattern separation in the dentate gyrus and CA3 of the hippocampus (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-02-17
    Description: Theoretical models have long pointed to the dentate gyrus as a possible source of neuronal pattern separation. In agreement with predictions from these models, we show that minimal changes in the shape of the environment in which rats are exploring can substantially alter correlated activity patterns among place-modulated granule cells in the dentate gyrus. When the environments are made more different, new cell populations are recruited in CA3 but not in the dentate gyrus. These results imply a dual mechanism for pattern separation in which signals from the entorhinal cortex can be decorrelated both by changes in coincidence patterns in the dentate gyrus and by recruitment of nonoverlapping cell assemblies in CA3.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leutgeb, Jill K -- Leutgeb, Stefan -- Moser, May-Britt -- Moser, Edvard I -- New York, N.Y. -- Science. 2007 Feb 16;315(5814):961-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for the Biology of Memory, Norwegian University of Science and Technology, 7489 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17303747" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dentate Gyrus/cytology/*physiology ; Hippocampus/cytology/*physiology ; Male ; Neurons/physiology ; Orientation/physiology ; Rats ; Rats, Long-Evans ; Space Perception/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    IRE1 signaling affects cell fate during the unfolded protein response (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-11-10
    Description: Endoplasmic reticulum (ER) stress activates a set of signaling pathways, collectively termed the unfolded protein response (UPR). The three UPR branches (IRE1, PERK, and ATF6) promote cell survival by reducing misfolded protein levels. UPR signaling also promotes apoptotic cell death if ER stress is not alleviated. How the UPR integrates its cytoprotective and proapoptotic outputs to select between life or death cell fates is unknown. We found that IRE1 and ATF6 activities were attenuated by persistent ER stress in human cells. By contrast, PERK signaling, including translational inhibition and proapoptotic transcription regulator Chop induction, was maintained. When IRE1 activity was sustained artificially, cell survival was enhanced, suggesting a causal link between the duration of UPR branch signaling and life or death cell fate after ER stress. Key findings from our studies in cell culture were recapitulated in photoreceptors expressing mutant rhodopsin in animal models of retinitis pigmentosa.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670588/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670588/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Jonathan H -- Li, Han -- Yasumura, Douglas -- Cohen, Hannah R -- Zhang, Chao -- Panning, Barbara -- Shokat, Kevan M -- Lavail, Matthew M -- Walter, Peter -- K08 EY018313/EY/NEI NIH HHS/ -- K08 EY018313-01/EY/NEI NIH HHS/ -- R01 EY020846/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 2007 Nov 9;318(5852):944-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, CA 94158, USA. Jonathan.Lin@ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17991856" target="_blank"〉PubMed〈/a〉
    Keywords: Activating Transcription Factor 6/metabolism ; Animals ; Animals, Genetically Modified ; *Apoptosis ; Cell Line ; *Cell Survival ; Disease Models, Animal ; Endoplasmic Reticulum/*metabolism ; Endoribonucleases/genetics/*metabolism ; Humans ; Kinetics ; Membrane Proteins/genetics/*metabolism ; Mice ; Mutation ; *Protein Folding ; Protein-Serine-Threonine Kinases/genetics/*metabolism ; Proteins/chemistry/*metabolism ; Rats ; Retina/metabolism ; Retinitis Pigmentosa/metabolism ; Rhodopsin/chemistry/metabolism ; *Signal Transduction ; eIF-2 Kinase/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Nucleus accumbens D2/3 receptors predict trait impulsivity and cocaine reinforcement (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-03-03
    Description: Stimulant addiction is often linked to excessive risk taking, sensation seeking, and impulsivity, but in ways that are poorly understood. We report here that a form of impulsivity in rats predicts high rates of intravenous cocaine self-administration and is associated with changes in dopamine (DA) function before drug exposure. Using positron emission tomography, we demonstrated that D2/3 receptor availability is significantly reduced in the nucleus accumbens of impulsive rats that were never exposed to cocaine and that such effects are independent of DA release. These data demonstrate that trait impulsivity predicts cocaine reinforcement and that D2 receptor dysfunction in abstinent cocaine addicts may, in part, be determined by premorbid influences.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892797/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1892797/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dalley, Jeffrey W -- Fryer, Tim D -- Brichard, Laurent -- Robinson, Emma S J -- Theobald, David E H -- Laane, Kristjan -- Pena, Yolanda -- Murphy, Emily R -- Shah, Yasmene -- Probst, Katrin -- Abakumova, Irina -- Aigbirhio, Franklin I -- Richards, Hugh K -- Hong, Young -- Baron, Jean-Claude -- Everitt, Barry J -- Robbins, Trevor W -- 076244/Wellcome Trust/United Kingdom -- G0001354/Medical Research Council/United Kingdom -- G0401068/Medical Research Council/United Kingdom -- G0600196/Medical Research Council/United Kingdom -- G0600986/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Mar 2;315(5816):1267-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Behavioral and Clinical Neuroscience Institute, University of Cambridge, Downing Street, Cambridge CB2 3EB, UK. jwd20@cam.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17332411" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basal Ganglia/metabolism/radionuclide imaging ; Benzamides/metabolism ; Cocaine/*administration & dosage ; *Cocaine-Related Disorders/metabolism/psychology ; Corpus Striatum/metabolism/radionuclide imaging ; Dopamine/metabolism ; Dopamine Antagonists/metabolism/pharmacology ; *Impulsive Behavior ; Male ; Nucleus Accumbens/*metabolism/radionuclide imaging ; Positron-Emission Tomography ; Pyrrolidines/metabolism ; Rats ; Reaction Time ; Receptors, Dopamine D2/*metabolism ; Receptors, Dopamine D3/*metabolism ; *Reinforcement (Psychology) ; Self Administration ; Synaptic Transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Sirtuin 2 inhibitors rescue alpha-synuclein-mediated toxicity in models of Parkinson's disease (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-26
    Description: The sirtuins are members of the histone deacetylase family of proteins that participate in a variety of cellular functions and play a role in aging. We identified a potent inhibitor of sirtuin 2 (SIRT2) and found that inhibition of SIRT2 rescued alpha-synuclein toxicity and modified inclusion morphology in a cellular model of Parkinson's disease. Genetic inhibition of SIRT2 via small interfering RNA similarly rescued alpha-synuclein toxicity. Furthermore, the inhibitors protected against dopaminergic cell death both in vitro and in a Drosophila model of Parkinson's disease. The results suggest a link between neurodegeneration and aging.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Outeiro, Tiago Fleming -- Kontopoulos, Eirene -- Altmann, Stephen M -- Kufareva, Irina -- Strathearn, Katherine E -- Amore, Allison M -- Volk, Catherine B -- Maxwell, Michele M -- Rochet, Jean-Christophe -- McLean, Pamela J -- Young, Anne B -- Abagyan, Ruben -- Feany, Mel B -- Hyman, Bradley T -- Kazantsev, Aleksey G -- 5P50-NS38372A-06/NS/NINDS NIH HHS/ -- R01-NS049221/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2007 Jul 27;317(5837):516-9. Epub 2007 Jun 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Alzheimer's Research Unit, MGH, Harvard Medical School, CNY 114, 16th Street, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17588900" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Animals, Genetically Modified ; Cell Death/drug effects ; Cell Line, Tumor ; Cells, Cultured ; Disease Models, Animal ; Dopamine/physiology ; Dose-Response Relationship, Drug ; Drosophila melanogaster ; Furans/*pharmacology ; Humans ; Models, Molecular ; Neurons/cytology/drug effects ; Parkinson Disease/*drug therapy/metabolism/pathology/*physiopathology ; Protein Conformation ; Quinolines/*pharmacology ; RNA, Small Interfering/genetics ; Rats ; Sirtuin 1 ; Sirtuin 2 ; Sirtuins/*antagonists & inhibitors/chemistry/genetics/*metabolism ; Transfection ; Tubulin/metabolism ; alpha-Synuclein/genetics/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    How synaptotagmin promotes membrane fusion (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-05-05
    Description: Synaptic vesicles loaded with neurotransmitters are exocytosed in a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-dependent manner after presynaptic depolarization induces calcium ion (Ca2+) influx. The Ca2+ sensor required for fast fusion is synaptotagmin-1. The activation energy of bilayer-bilayer fusion is very high (approximately 40 k(B)T). We found that, in response to Ca2+ binding, synaptotagmin-1 could promote SNARE-mediated fusion by lowering this activation barrier by inducing high positive curvature in target membranes on C2-domain membrane insertion. Thus, synaptotagmin-1 triggers the fusion of docked vesicles by local Ca2+-dependent buckling of the plasma membrane together with the zippering of SNAREs. This mechanism may be widely used in membrane fusion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martens, Sascha -- Kozlov, Michael M -- McMahon, Harvey T -- MC_U105178795/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 May 25;316(5828):1205-8. Epub 2007 May 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council-Laboratory of Molecular Biology, Hills Road, CB2 0QH Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17478680" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*physiology ; Cell Membrane/*physiology/ultrastructure ; Exocytosis/physiology ; Humans ; Liposomes ; Membrane Fusion ; Models, Biological ; Rats ; SNARE Proteins/*physiology ; Synaptic Vesicles/*physiology/ultrastructure ; Synaptotagmin I/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Embryonic stem cells. Stem cell science advances as politics stall (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-06-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holden, Constance -- New York, N.Y. -- Science. 2007 Jun 29;316(5833):1825.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17600188" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Cloning, Organism ; Embryo Implantation ; Embryo Research/ethics/legislation & jurisprudence ; Embryo, Mammalian ; Embryonic Development ; *Embryonic Stem Cells/cytology/physiology ; Humans ; Mice ; *Pluripotent Stem Cells/cytology ; Politics ; Rats
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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