GABAA receptor-mediated K(+)-evoked GABA release from globus pallidus--analysis using microdialysis

Presynaptic modulation of gamma-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 released from the globus pallidus. GABA release from the globus pallidus was also augmented dose-dependently by the addition of KCI. Muscimol, a GABAA 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 GABAA receptor antagonist. On the other hand, baclofen, a GABAB receptor agonist, did not induce any significant changes in the 100 mM KCl-evoked GABA release. Similarly, 3-aminopropylphosphonous acid, a GABAB 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 GABAB 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 GABAA autoreceptor.