Linked Life Data

1980647

Source:http://linkedlifedata.com/resource/pubmed/id/1980647

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4-5
pubmed:dateCreated
1991-3-11
pubmed:abstractText
The effects of glutamate and other more selective excitatory amino acid (EAA) analogs on intracellular free calcium concentration ( [Ca2+]i) were examined in Fura 2-loaded cultured chick embryo cortical cells (90% neuronal). Four EAA receptors were evident in these studies: an N-methyl-D-aspartate (NMDA) receptor, a kainate receptor, and two quisqualate receptors. The [Ca2+]i response to NMDA was blocked or reversed by selective antagonists such as 2-amino-5-phosphonovalerate (APV), MK801 and ketamine, as well as by desmethylimipramine and dextromethorphan. Glycine potentiated the [Ca2+]i response to NMDA, and high concentrations of glycine selectively overcame blockade by kynurenic acid, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and cis-piperidine-2,3-dicarboxylic acid (PDA). The [(Ca2+]i response to kainate was generally larger than the NMDA response, and the kainate response desensitized slightly over the first minute. CNQX was more potent as an antagonist of the kainate response than of the NMDA response, even in the absence of added glycine; kynurenic acid and PDA conversely had little effect on the kainate response in these cells at concentrations which blocked the NMDA response. The desensitization of the [Ca2+]i response to kainate was greatly augmented by quisqualate and by the putative ionotropic quisqualate receptor agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). In the absence of kainate, both quisqualate and AMPA increased [Ca2+]i though less so than did NMDA or kainate. Quisqualate (and AMPA and glutamate) were not acting as partial agonists at the kainate receptor, since the potency of these agonists in reversing the kainate [Ca2+]i response was independent of kainate concentration. Quisqualate, but not AMPA, also produced a small increase in [Ca2+]i which preceded the negative effect of this agonist on the kainate response. This increase in [Ca2+]i could also be evoked by quisqualate or glutamate after inhibition of the kainate response by AMPA. Quisqualate and glutamate, but not the other EAA agonists, also increased [Ca2+]i after chelation of extracellular calcium with EGTA. This effect appears to be mediated by the metabotropic quisqualate receptor. These cells should provide a useful system for studying regulation and interactions of EAA receptors, and for screening drugs which might act at these receptors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
189
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
253-66
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Characterization of Ca2(+)-mobilizing excitatory amino acid receptors in cultured chick cortical cells.
pubmed:affiliation
Department of Psychiatry, Tufts University School of Medicine, New England Medical Center, Boston, MA 02111.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't