pubmed-article:14622176 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C0206441 | lld:lifeskim |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C1521828 | lld:lifeskim |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
pubmed-article:14622176 | lifeskim:mentions | umls-concept:C0598352 | lld:lifeskim |
pubmed-article:14622176 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:14622176 | pubmed:dateCreated | 2003-11-18 | lld:pubmed |
pubmed-article:14622176 | pubmed:abstractText | The main inhibitory neurotransmitter in the mammalian forebrain is gamma-amino butyric acid (GABA), which acts through A and B type receptors. GABAA receptors mediate inhibition via an increase in membrane conductance (shunting) and/or membrane potential hyperpolarization. Shunting inhibition is thought to decrease the gain between neural input and output, and thus to act as a divisor, but may do so only below the spike threshold. To investigate the role of shunting inhibition in neocortical neurons, whole-cell patch-clamp recordings were obtained from layer V pyramidal cells of somatosensory cortex in juvenile rats. Sub- and suprathreshold voltage responses were elicited by somatic step current injections and a shunting conductance was generated via a dynamic clamp. Increasing the dynamic clamp shunting conductance led to a parallel shift of the current-discharge curves and a reduced slope of the current-voltage relationship, i.e. a decrease of neural gain. Selective activation of GABAAA receptors with the competitive agonist isoguvacine or rises of endogenous GABA with the specific reuptake blocker nipecotic acid led to a proportional decrease of subthreshold membrane voltage, but a constant offset of discharge rates, thus acting like a shunting conductance. Similarly, isoguvacine and nipecotic acid decreased the gain of excitatory postsynaptic potentials. In all three experimental conditions, shunting inhibition divisively affected subthreshold voltages, while the time-averaged suprathreshold membrane potential was offset by a constant amount. I conclude that shunting inhibition in pyramidal cells has a dual impact on neural output: it is divisive for subthreshold voltages but subtractive for spike frequencies. | lld:pubmed |
pubmed-article:14622176 | pubmed:language | eng | lld:pubmed |
pubmed-article:14622176 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:14622176 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:14622176 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:14622176 | pubmed:month | Oct | lld:pubmed |
pubmed-article:14622176 | pubmed:issn | 0953-816X | lld:pubmed |
pubmed-article:14622176 | pubmed:author | pubmed-author:UlrichDanielD | lld:pubmed |
pubmed-article:14622176 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:14622176 | pubmed:volume | 18 | lld:pubmed |
pubmed-article:14622176 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:14622176 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:14622176 | pubmed:pagination | 2159-65 | lld:pubmed |
pubmed-article:14622176 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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pubmed-article:14622176 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:14622176 | pubmed:articleTitle | Differential arithmetic of shunting inhibition for voltage and spike rate in neocortical pyramidal cells. | lld:pubmed |
pubmed-article:14622176 | pubmed:affiliation | Institute of Physiology, University of Bern, Bühlplatz 5, CH-3012 Bern, Switzerland. ulrich@pyl.unibe.ch | lld:pubmed |
pubmed-article:14622176 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:14622176 | pubmed:publicationType | Comparative Study | lld:pubmed |
pubmed-article:14622176 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:14622176 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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