Abstract— Elevated K+0 elicited a substantial Ca‐independent efflux of accumulated GABA from cortical synaptosomal fractions. Efflux from tissue labelled with either NE or choline was affected considerably less by elevated K+ pulses in the absence of calcium. K‐facilitated Ca‐dependent efflux was large for all three of the accumulated substances. K‐dependent (Ca‐independent) efflux of accumulated GABA was associated with all subcellular fractions exhibiting GABA accumulation whereas K‐facilitated Ca‐dependent efflux was restricted to fractions containing synaptosomes. Eighty per cent of both GABA accumulation and K‐dependent efflux was, however, recovered in a purified synaptosomal fraction. Alanine slightly decreased GABA accumulation, but % K‐dependent efflux was not affected. Elevated K+, in the absence of calcium, released GABA from accumulated pools in preference to endogenous pools, whereas the Ca‐dependent efflux, facilitated by K+, was similar for both accumulated and endogenous GABA. The Ca‐independent efflux of accumulated GABA increased linearly with log (K+)0 between 10 and 70 mM‐K+ in sodium‐containing media. Prior treatment with veratridine or Na‐free medium substantially decreased the Ca‐independent but not the Ca‐dependent GABA efflux produced by elevated K+ pulses. The Ca‐dependent and Ca‐independent efflux of accumulated GABA in response to elevated K+ pulses is suggested to arise not only via different flux mechanisms but also from different GABA pools. The Ca‐dependent efflux is interpreted to reflect stimulus‐secretion coupling processes whereas the Ca‐independent efflux may reflect membrane transport processes.
Journal of Neurochemistry – Wiley
Published: May 1, 1978
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