GABA A receptor-mediated k +-evoked gaba release from globus pallidus—analysis using microdialysis

Abstract

Presynaptic modulation of γ-aminobutyric acid (GABA) release in the globus pallidus of rat was examined using in vivo microdialysis procedures. The addition of nipecotic acid (0.5 mM), a neuronal GABA uptake inhibitor, into perfusate, resulted in an increase in the basal GABA release from the globus pallidus. GABA release from the globus pallidus was also augmented dose-dependently by the addition of KCl. Muscimol, a GABA A receptor agonist, caused a significant suppression of the high potassium (100 mM)-evoked release of GABA, and this suppressive effect of muscimol was antagonized invariably by bicuculline, a GABA A receptor antagonist. On the other hand, baclofen, a GABA B receptor agonist, did not induce any significant changes in the 100 mM KCl-evoked GABA release. Similarly, 3-aminopropylphosphonous acid, a GABA B receptor agonist, failed to suppress the GABA release induced by high (100 mM) and low (50 mM) concentrations of KCl from the globus pallidus. Furthermore, CGP 54626A, a GABA B receptor antagonist, had no significant effect on these KCl-evoked GABA releases. These results suggest that presynaptic modulation of GABA release in the globus pallidus may be mediated by the GABA A autoreceptor.