K+ differentially affects the excitatory amino acids- and carbachol-elicited inositol phosphate formation in rat brain synaptoneurosomes.

K+, excitatory amino acids (EAAs) and carbachol (Carb) were tested separately or in pairs for their ability to stimulate inositol phosphate (IPs) formation in rat forebrain synaptoneurosomes. K+ ions per se, stimulate IPs synthesis (158% of the control value) as well as EAAs and Carb. The glutamate (Glu)- and quisqualate (QA)-elicited IPs formation is not additive with that evoked by K+.

A new quisqualate receptor subtype (sAA(2)) responsible for the glutamate-induced inositol phosphate formation in rat brain synaptoneurosomes.

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); ?-d-glutamyl-glycine (?-DGG)] known to inhibit the QA-induced depolarization.

Characterization of subtypes of excitatory amino acid receptors involved in the stimulation of inositol phosphate synthesis in rat brain synaptoneurosomes.

The action of excitatory amino acids (EAA) on inositol phosphates (IPs) synthesis was examined in forebrain synaptoneurosomes of Long Evans rats (6-9 days old). Glutamate (GLU) (EC50: 23 microM) and quisqualate (QA) (EC50: 0.12 microM) enhanced IPs turnover.