Effect of Cholecystokinin Octapeptide on Endogenous Amino Acid Release from the Rat Ventromedial Nucleus of the Hypothalamus and Striatum

Abstract

The sulphated octapeptide of cholecystokinin (CCK-8S) was found to cause a dose-dependent increase in the basal release of aspartate, glycine, and γ-aminobutyric acid from the striatum and the ventromedial nucleus of the hypothalamus (VMH). No effect on amino acid release was observed after electrical (VMH) or potassium (striatum) stimulation. Experiments performed using the CCK_B-selective antagonist L-365,260 and the CCK_A-selective antagonist L-364,718 suggested that this action of CCK-8S was mediated via the CCK_B receptor. The ability of CCK-8S to evoke amino acid release was not dependent on the presence of extracellular calcium, though the effect was abolished by tetrodotoxin. Inhibition of protein kinase activity by staurosporine prevented the excitatory effects of CCK-8S on amino acid release.