Taurocyamine specifically stimulates γ-aminobutyric acid release.

Abstract

We previously reported that threshold for occurrence of cysteine sulfinic acid (CSA)-induced seizure discharge on EEG was lowered in the taurocyamine-treated rats and that i.c.v. injection of taurocyamine caused seizure discharge which was prevented by simultaneous injection of γ-aminobutyric acid (GABA). In this paper, we studied the effect of taurocyamine on the release of GABA in rat brain slices and P2 fraction. Superfusion with 0.1-10 mM taurocyamine caused a dose-dependent, Ca2+-independent increase in the release of 3H-GABA from preloaded slices and P2 fraction of rat cerebral cortex. This effect was specific for GABA since taurocyamine had no effect on the release of 3H-glutamate and 3H-acetylcholine. Taurocyamine (10 mM) did not affect high potassium-induced release of 3H-GABA. The release of endogenous GABA was also stimulated by taurocyamine (5 mM) or a depolarizing concentration of potassium. GABA (10 μM) caused 50% inhibition of 3H-glutamate release from hippocampal slices in normal rats, whereas it did not alter the release in taurocyamine-treated rats, indicating decreased sensitivity to GABA in the treated rats.