Abstract
The effects of γ-aminobutyric acid (GABA) and benzodiazepines on the electrical activity of cultured frog melanotrophs were studied using the patch-clamp technique. In the cell-attached configuration, the exposure to GABA caused a blockage of the spontaneous firing. In the whole-cell configuration, with physiological chloride concentrations, GABA evoked a hyperpolarization associated with a decrease of membrane resistance, generating an inward chloride current. Clonazepam, a central-type benzodiazepine agonist, potentiated the GABA-induced current and the resulting hyperpolarization. In addition, the benzodiazepine inverse agonist Ro 19-4603 totally abolished GABA-induced hyperpolarizing chloride current. Since the pars intermedia of the frog pituitary is composed of a ‘pure’ population of endocrine cells enriched with GABA A receptors, our results indicate that these cells represent a valuable model in which to investigate the electrophysiological effects of ligands for the GABA A benzodiazepine receptor complex.
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