EFFECT OF CHOLECYSTOKININ OCTAPEPTIDE ON ENDOGENOUS AMINO-ACID RELEASE FROM THE RAT VENTROMEDIAL NUCLEUS OF THE HYPOTHALAMUS AND STRIATUM

The sulphated octapeptide of cholecystokinin (CCK-8S) was found to cause a dose-dependent increase in the basal release of asparate, glycine, and gamma-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.