| Presynaptic kainate receptor activation preserves asynchronous GABA release despite the reduction in synchronous release from hippocampal cholecystokinin interneurons. | |
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MedLine Citation:
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PMID: 20720128 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Inhibitory synaptic transmission in the hippocampus in mediated by a wide variety of different interneuron classes which are assumed to play different roles in network activity. Activation of presynaptic kainate receptors (KARs) has been shown to reduce inhibitory transmission but the interneuron class(es) at which they act is only recently beginning to emerge. Using paired recordings we show that KAR activation causes a decrease in presynaptic release from cholecystokinin (CCK)- but not parvalbumin-containing interneurons and that this decrease is observed when pyramidal cells, but not interneurons, are the postsynaptic target. We also show that although the synchronous release component is reduced, the barrage of asynchronous GABA release from CCK interneurons during sustained firing is unaffected by KAR activation. This indicates that presynaptic KARs preserve and act in concert with asynchronous release to switch CCK interneurons from a phasic inhibition mode to produce prolonged inhibition during periods of intense activity. |
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Authors:
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Michael I Daw; Kenneth A Pelkey; Ramesh Chittajallu; Chris J McBain |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, N.I.H., Intramural |
Journal Detail:
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Title: The Journal of neuroscience : the official journal of the Society for Neuroscience Volume: 30 ISSN: 1529-2401 ISO Abbreviation: J. Neurosci. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-08-19 Completed Date: 2010-09-03 Revised Date: 2011-07-22 |
Medline Journal Info:
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Nlm Unique ID: 8102140 Medline TA: J Neurosci Country: United States |
Other Details:
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Languages: eng Pagination: 11202-9 Citation Subset: IM |
Affiliation:
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Program in Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Developmental Synaptic Plasticity Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA. michael.daw@ed.ac.uk |
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| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials
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physiology Animals Cholecystokinin / metabolism* Hippocampus / physiology* Inhibitory Postsynaptic Potentials / physiology Interneurons / physiology* Kainic Acid / metabolism Mice Mice, Inbred C57BL Mice, Transgenic Neural Inhibition / physiology Parvalbumins / metabolism Presynaptic Terminals / physiology* Pyramidal Cells / physiology Receptor, Cannabinoid, CB1 / metabolism Receptors, GABA-B / metabolism Receptors, Kainic Acid / metabolism* Synaptic Transmission / physiology gamma-Aminobutyric Acid / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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Z01 HD001205-15/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Gluk1 kainate receptor; 0/Parvalbumins; 0/Receptor, Cannabinoid, CB1; 0/Receptors, GABA-B; 0/Receptors, Kainic Acid; 487-79-6/Kainic Acid; 56-12-2/gamma-Aminobutyric Acid; 9011-97-6/Cholecystokinin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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