A possible neuronal release of [14C] GABA from the rat cerebellum in vivo

Release patterns for exogenously applied [¹⁴C] labelled -amino-n-butyric-acid (GABA) have been investigated in rat cerebellar cortex in vivo. An increase in [¹⁴C] GABA release could be evoked by stimulating with high (40 mM) K⁺ or veratridine (10^–4 M) but not with direct electrical stimulation. Biphasic patterns for high K⁺ and possibly veratridine stimulated release of GABA suggest the existence of two separate anatomical sources of isotope which are sensitive to these depolarising stimuli. Both K⁺ and veratridine-evoked GABA release are calcium dependent. Studies involving partial replacement of Na⁺ with HEPES, (N-2-hydroxyethyl-piperazine-N-2-ethane-sulphonic acid), sucrose or choline chloride also reveal a sodium dependency of [¹⁴C] GABA release. These studies collectively indicate a neuronal source for evoked GABA release, a criterion for transmitter identification not previously satisfied in the cerebellar cortex.Supported in part by a grant from S.R.C. to N.D. and C.G.D.Supported by CAPES and FAPESP (Brazil)Supported by CNPq and FAPESP (Brazil)