Differential effects of veratridine and potassium depolarization on neuronal and glial GABA release

Abstract

The effect of veratridine and potassium depolarization on the release of [3H]GABA from neural tissues in which GABA uptake is neuronal (cerebrocortical slices and frog retina) or glial (rat retina, spinal and sympathetic ganglia) was studied. The 'neuronal' but not the 'glial' release of [3H]GABA was greatly increased by KC1 (25 mM) and veratridine (10 microM). The 'neuronal' release of [3H]GABA evoked with KC1 was calcium dependent but the small potassium induced increase in 'glial' release were not reduced in the absence of calcium ions even when additional Mg2+ was included in the medium. Surprisingly, the veratridine induced release of [3H]GABA from cortical slices was greatly potentiated in calcium free medium although the release of [3H]noradrenaline produced by veratridine was calcium dependent. Because of the insensitivity of the glial GABA release mechanism to potassium depolarization, it is concluded that release of endogenous GABA from glial pools in response to physiological increases in extracellular potassium is unlikely to be important.