The glutamate inhibition of carbachol stimulated inositol phosphate production in rat cortical cells is mediated through an ionotropic NMDA receptor.
Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP1) (3-4 fold of basal, P < 0.001) in fetal rat cortical cells is attenuated by glutamate (at 0.1 mM, 40-70% of carbachol alone, P < 0.001). This inhibition by glutamate was reduced by 2-amino-5-phosphonopentanoic acid (AP5), but not by gamma-D-glutamylaminomethyl sulphonic acid (GAMS) [corrected] or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic receptor agonist (1S,3R)-1-aminocyclopentane-1-3-dicarboxylic acid [(1S,3R)-ACPD] (up to 0.1 mM) had no effect upon carbachol stimulated IP1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP1, by glutamate in rat cortical cells is mediated through an NMDA ionotropic receptor.
Ham
J
J
Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff, UK.
Scanlon
M
M
D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism*; D005333:Fetus; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D007295:Inositol Phosphates / Q000037:antagonists & inhibitors*; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*
D005971:Glutamates; D007295:Inositol Phosphates; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D002217:Carbachol