In a recent study, Roberto et al. (2008) reported neuroadaptations in GABAB receptors in CeA after chronic EtOH exposure. The sensitivity of GABA IPSCs to the GABAB receptor antagonist CGP 55845A and agonist baclofen was decreased after chronic EtOH, suggesting downregulation of this system. Specifically, the GABAB receptor antagonist, CGP 55845A significantly increased the mean amplitude of evoked IPSCs (by 12 ± 5%) in CeA from naïve rats. This increase in the IPSC amplitude was associated with a significant decrease in PPF, suggesting a tonic activation of presynaptic GABAB receptors in naïve rats. In contrast, in CeA from EtOH-dependent rats, CGP 55845A did not alter the mean evoked IPSCs (98 ± 4%) and did not affect mean PPF. Baclofen (10 µM) markedly depressed evoked GABA-IPSC amplitudes in neurons of naïve rats (to 38% of control), with recovery during washout. The baclofen-induced inhibition of GABA IPSCs was significantly reduced (to 86% of control) in neurons of EtOH-dependent rats. In addition, in CeA neurons from EtOH-dependent rats, baclofen-induced depression was associated with a smaller increase of the PPF ratio of GABA IPSCs
