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  • Rats
  • American Association for the Advancement of Science (AAAS)  (29)
  • American Chemical Society
  • American Chemical Society (ACS)
  • American Institute of Physics (AIP)
  • PANGAEA
  • 2005-2009  (29)
  • 1995-1999
  • 1975-1979
  • 2008  (29)
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  • American Association for the Advancement of Science (AAAS)  (29)
  • American Chemical Society
  • American Chemical Society (ACS)
  • American Institute of Physics (AIP)
  • PANGAEA
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  • 2005-2009  (29)
  • 1995-1999
  • 1975-1979
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  • 1
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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
    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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  • 2
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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
    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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    A model for neuronal competition during development (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
    Print ISSN: 0036-8075
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  • 5
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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
    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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    Neuroscience. Refreshing connections (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
    Print ISSN: 0036-8075
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  • 8
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    Leiomodin is an actin filament nucleator in muscle cells (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 9
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    Bioactive contaminants leach from disposable laboratory plasticware (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 10
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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
    Print ISSN: 0036-8075
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  • 11
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    Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 12
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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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  • 13
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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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  • 14
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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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  • 15
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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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  • 16
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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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  • 17
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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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  • 18
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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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  • 19
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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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  • 20
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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)
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    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
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 21
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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
    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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  • 22
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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
    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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  • 23
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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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 24
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    Video-rate far-field optical nanoscopy dissects synaptic vesicle movement (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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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  • 25
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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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  • 26
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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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  • 27
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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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  • 28
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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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  • 29
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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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