A possible neuronal release of [14C] GABA from the rat cerebellum in vivo.
Release patterns for exogenously applied [14C] labelled alpha-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.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002525:Cerebellar Cortex / Q000378:metabolism*; D004558:Electric Stimulation; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D005680:gamma-Aminobutyric Acid; D014701:Veratridine; D012964:Sodium; D011188:Potassium; D002118:Calcium