Ethanol potentiation of GABA-induced electrophysiological responses in cerebellum: requirement for catecholamine modulation

In this study, we confirmed that microiontophoretically applied norepinephrine (NE) and isoproterenol potentiate the depressant effects of locally-applied γ-aminobutyric acid (GABA) on cerebellar Purkinje neurons of anesthetized rats. Although ethanol (EtOH) does not reliably or efficaciously potentiate GABA-induced depressions of neuronal activity, we found that systemic or locally-applied EtOH does markedly potentiate GABA-induced inhibitions of Purkinje neuron firing rate if that response is concomitantly modulated by NE or isoproterenol. This study suggests that the EtOH sensitivity of the GABA mechanism of electrophysiological responses in the cerebellar cortex is regulated by the neuromodulatory effect of β-adrenergic receptor activation.