Is GABA release modulated by presynaptic receptors?

Abstract

THERE is considerable evidence, in both the peripheral and central nervous systems, that presynaptic α-adrenoreceptors modulate noradrenaline release induced by both electrical and potassium ion stimulation; α-agonists inhibit and α-antagonists facilitate this release^1–5. There is also evidence that similar control mechanisms occur in dopaminergic^4,6–9 and cholinergic¹⁰ neurones. Here we report that the release of γ-aminobutyric acid (GABA) from in vitro rat frontal cortex, caused by elevated potassium ion concentrations, is reduced by the GABA agonists muscimol and 3-aminopropane sulphonic acid, and by GABA itself, and also that the effect of muscimol is antagonised by the GABA antagonists bicuculline and picrotoxin. This in vitro study demonstrates that the release of GABA is subject to a negative feedback control which may be important in vivo, and further, that this mechanism can be modified by drugs.