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Abstract
Carbachol (0.1 mM) stimulated accumulation of inositol monophosphate (IP 1) (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 γ- d-SCPnic acid (GAMS) 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 IP 1. Staurosporine and quinacrine were unable to prevent the inhibition of carbachol stimulated IP1 by glutamate. These data suggest that the inhibition of carbachol-stimulated IP 1, by glutamate in rat cortical cells is mediated through an NMDA ionotropic receptor.
Published Version
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