| pubmed-article:1403103 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C0206441 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:1403103 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:1403103 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:1403103 | pubmed:dateCreated | 1992-11-18 | lld:pubmed |
| pubmed-article:1403103 | pubmed:abstractText | Using intracellular recording techniques in CA1 cells in the hippocampal slice, we studied the responses of cells to synaptically released and iontophoretically applied GABA. With high-resistance, Cl(-)-filled electrodes, which inverted and enlarged the responses at normal resting potentials, we examined spontaneous GABA-mediated IPSPs. Usually we recorded the spontaneous events in the presence of carbachol (10-25 microM), which significantly increased IPSP frequency and blocked potentially confounding K+ conductances. Following a train of action potentials, spontaneous IPSPs were transiently suppressed. This suppression could not be accounted for by membrane conductance changes following the train or activation of a recurrent circuit. Whole-cell voltage-clamp recordings in the slice indicated that the amplitudes of the spontaneous GABAA inhibitory postsynaptic currents (IPSCs) were also diminished following the action potential train. In some cases BAY K 8644, a Ca2+ channel agonist, enhanced the suppression of IPSPs, while buffering changes in [Ca2+]i with EGTA or BAPTA prevented it. The monosynaptically evoked IPSC in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and dl-2-amino-5-phosphonovaleric acid (APN) was also diminished following a train of action potentials; however, iontophoretically applied GABA responses did not change significantly. These studies suggest that localized physiological changes in postsynaptic [Ca2+]i potently modulate synaptic GABAA inputs and that this modulation may be an important regulatory mechanism in mammalian brain. | lld:pubmed |
| pubmed-article:1403103 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1403103 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1403103 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1403103 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1403103 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1403103 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1403103 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1403103 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1403103 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:1403103 | pubmed:issn | 0270-6474 | lld:pubmed |
| pubmed-article:1403103 | pubmed:author | pubmed-author:AlgerB EBE | lld:pubmed |
| pubmed-article:1403103 | pubmed:author | pubmed-author:PitlerT ATA | lld:pubmed |
| pubmed-article:1403103 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1403103 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:1403103 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1403103 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1403103 | pubmed:pagination | 4122-32 | lld:pubmed |
| pubmed-article:1403103 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:meshHeading | pubmed-meshheading:1403103-... | lld:pubmed |
| pubmed-article:1403103 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1403103 | pubmed:articleTitle | Postsynaptic spike firing reduces synaptic GABAA responses in hippocampal pyramidal cells. | lld:pubmed |
| pubmed-article:1403103 | pubmed:affiliation | Department of Physiology, University of Maryland School of Medicine, Baltimore 21201. | lld:pubmed |
| pubmed-article:1403103 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1403103 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1403103 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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