| pubmed-article:7527076 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7527076 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:7527076 | lifeskim:mentions | umls-concept:C0220839 | lld:lifeskim |
| pubmed-article:7527076 | lifeskim:mentions | umls-concept:C0439834 | lld:lifeskim |
| pubmed-article:7527076 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:7527076 | lifeskim:mentions | umls-concept:C0871161 | lld:lifeskim |
| pubmed-article:7527076 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:7527076 | pubmed:dateCreated | 1994-12-30 | lld:pubmed |
| pubmed-article:7527076 | pubmed:abstractText | 1. Pyramidal neurons from layer V of rat neocortex were recorded intracellularly in a brain slice preparation to study their response to stimulation of metabotropic glutamate receptors (mGluRs) by bath application of the selective mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) and by the nonselective agonists glutamate and quisqualate. 2. The principal postsynaptic effect of mGluR stimulation in the presence of ionotropic glutaminergic and muscarinic cholinergic antagonists was the appearance of a slow afterdepolarization (ADP) after evoked spikes. Only an afterhyperpolarization (AHP) was present in control perfusate. After 20 spikes evoked individually at 100 Hz the ADP peaked at 317 +/- 117 (SD) ms after the spike train, ranged from 1 to 12 mV in peak amplitude, and decayed over 7.4 +/- 4.7 s. This effect was not blocked by L-2-amino-3-phosphono-propionic acid (1 mM). Spikes evoked in the presence of the ionotropic glutamate receptor agonist R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) did not have an ADP. 3. A detectable ADP appeared at concentrations of 0.1 microM quisqualate or 0.5 microM 1S,3R-ACPD. Maximum ADP amplitude was obtained with 5 microM quisqualate or 100 microM 1S,3R-ACPD. The ADP appeared after a single evoked spike in most cells tested and ADP amplitude increased to a maximum as the number of spikes evoked at 100 Hz was increased to between 5 and 20. 4. The ionic mechanisms underlying the ADP were examined by ion substitution and the application of channel-blocking agents. No difference in ADP amplitude was observed when the recording electrode contained CH3SO4. instead of Cl.. The ADP was present after 3 mM extracellular Cs+ were added to block the hyperpolarization-activated cation current or when 100 microM Ba2+ were included to block voltage-gated K+ currents. The ADP was abolished when Mn2+ was substituted for Ca2+ in the perfusate or when the Ca2+ chelator 5,5'-dimethyl-bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid was included in the recording electrode. A large ADP followed Ca2+ spikes evoked in the presence of 1 microM tetrodotoxin with 20 mM tetraethylammonium in the perfusate or with Cs+ substituted for K+ in the recording electrode. The amplitude of the ADP after the Ca2+ spikes was reduced by 49% when extracellular Na+ concentration was reduced from 136 to 26 mM. 5. The voltage dependence of the ADP was examined in relation to K+ equilibrium potential (EK).(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
| pubmed-article:7527076 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7527076 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:7527076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7527076 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7527076 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:7527076 | pubmed:issn | 0022-3077 | lld:pubmed |
| pubmed-article:7527076 | pubmed:author | pubmed-author:CrillW EWE | lld:pubmed |
| pubmed-article:7527076 | pubmed:author | pubmed-author:SchwindtP CPC | lld:pubmed |
| pubmed-article:7527076 | pubmed:author | pubmed-author:GreeneC CCC | lld:pubmed |
| pubmed-article:7527076 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7527076 | pubmed:volume | 72 | lld:pubmed |
| pubmed-article:7527076 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7527076 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7527076 | pubmed:pagination | 693-704 | lld:pubmed |
| pubmed-article:7527076 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:7527076 | pubmed:meshHeading | pubmed-meshheading:7527076-... | lld:pubmed |
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| pubmed-article:7527076 | pubmed:meshHeading | pubmed-meshheading:7527076-... | lld:pubmed |
| pubmed-article:7527076 | pubmed:meshHeading | pubmed-meshheading:7527076-... | lld:pubmed |
| pubmed-article:7527076 | pubmed:meshHeading | pubmed-meshheading:7527076-... | lld:pubmed |
| pubmed-article:7527076 | pubmed:meshHeading | pubmed-meshheading:7527076-... | lld:pubmed |
| pubmed-article:7527076 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7527076 | pubmed:articleTitle | Properties and ionic mechanisms of a metabotropic glutamate receptor-mediated slow afterdepolarization in neocortical neurons. | lld:pubmed |
| pubmed-article:7527076 | pubmed:affiliation | Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195. | lld:pubmed |
| pubmed-article:7527076 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7527076 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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