A new quisqualate receptor subtype (sAA2) responsible for the glutamate-induced inositol phosphate formation in rat brain synaptoneurosomes

Abstract

Inositol phosphate synthesis elicited by excitatory amino acids was measured in rat forebrain synaptoneurosomes in presence of Li+. Quisqualate (QA) was the most potent excitatory amino acid inducing inositol phosphate formation. This QA action was not blocked by any of the usual antagonists [glutamate-amino-methyl-sulphonate (GAMS); glutamate-diethyl-ester (GDEE); γ-d-glutamyl-glycine (γ-DGG)] known to inhibit the QA-induced depolarization. The same was found for the most potent and selective QA antagonist reported so far [6-nitro-7-cyanoquinoxaline-2,3-dion (FG 9065)]. In addition, dl-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) a potent depolarizing agonist at the quisqualate receptor subtype was about 300 times less potent than quisqualate in increasing inositol phosphate accumulation. Our results provide the first pharmacological evidence indicating that a new quisqualate receptor subtype, tentatively termed sAA2 is responsible for inositol phosphate formation. © 1988.