Potassium-stimulated release of [3H]taurine from cultured GABAergic and glutamatergic neurons.

The effect of depolarizing concentrations of potassium (56 mM) on the release of [3H]taurine was examined in two types of cultured neurons from mouse brain: cerebral cortex neurons, which are largely GABAergic, and cerebellar neurons, which after treatment with kainate consist almost entirely of glutamatergic granule cells. The release of [3H]taurine was compared to that of gamma-[3H]aminobutyric acid [( 3H]GABA) in cortical neurons and to that of D-[3H]aspartate in granule cells. Cortical neurons responded to potassium stimulation (1 min or continuously) by an immediate increase in [3H]GABA efflux of more than six times over the basal efflux, followed by a sharp decline despite the persistence of the stimulatory agent. The potassium-induced release of [3H]GABA was largely calcium-dependent. The release of [3H]taurine was considerably less in magnitude, only doubling after the stimulus, with a time course delayed in both onset and decline. The release of [3H]taurine was partially calcium-dependent and was also decreased in low-chloride solutions. In cerebellar granule cells, exposure to potassium resulted in a large (sixfold) and prompt release of D-[3H]aspartate, largely calcium-dependent. A totally different pattern was observed for the release of [3H]taurine. A stimulatory effect occurred only when cells were exposed continuously to potassium. Taurine efflux was very delayed, with a broad stimulus plateau reached after 15-20 min of stimulation. Taurine release was unaffected by omission of calcium, but it was abolished in a low-chloride medium. These results suggest that taurine is released from cells handling other neuroactive amino acids as neurotransmitters.(ABSTRACT TRUNCATED AT 250 WORDS)