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  • Rats  (15)
  • American Association for the Advancement of Science (AAAS)  (15)
  • American Physical Society
  • 2010-2014
  • 2005-2009  (15)
  • 1980-1984
  • 2008  (15)
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  • 2010-2014
  • 2005-2009  (15)
  • 1980-1984
Year
  • 1
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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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  • 2
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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
    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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    Electric fields due to synaptic currents sharpen excitatory transmission (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    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
    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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    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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  • 6
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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
    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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    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
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 8
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    Reward-predictive cues enhance excitatory synaptic strength onto midbrain dopamine neurons (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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  • 9
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    Identifying autism loci and genes by tracing recent shared ancestry (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 10
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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
    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)
    Location Call Number Expected Availability
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