THE GLUTAMATE INHIBITION OF CARBACHOL-STIMULATED INOSITOL PHOSPHATE PRODUCTION IN RAT CORTICAL-CELLS IS MEDIATED THROUGH AN IONOTROPIC NMDARECEPTOR (VOL 167, PG 63, 1994)

Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate ( IP1) (3-4-fold of basal, P < 0.001) in fetal rat cortical cells is att enuated by glutamate (at 0.1 mM, 40-70% of carbachol alone, P < 0.001) . This inhibition by glutamate was reduced by 2-amino-5-phosphonopenta noic acid (AP5), but not by gamma-D-glutamylaminomethyl sulphonic acid (GAMS) or 2-amino-3-phosphonopropionic acid (AP3). The metabotropic r eceptor 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 in hibition of carbachol-stimulated IP1, by glutamate in rat cortical cel ls is mediated through an NMDA ionotropic receptor.