Roberto et al. (2004a) recently assessed whether GABAergic synaptic changes occur with EtOH-dependence in rat central amygdala (CeA) slices. To obtain dependent rats, these investigators used an EtOH vapor inhalation method (Rogers et al. 1979). In this study, male Sprague–Dawley rats were exposed to a continuous EtOH vapor for 2–3 weeks with a targeted blood alcohol level of 150–200 mg/dL. Control rats were maintained in similar chambers without EtOH vapor. On experiment days, the chronic EtOH-treated rats were maintained in the EtOH vapor chamber until preparation of the CeA slices, and recordings of GABAergic transmission were made in EtOH-free solution 2–8 h after cutting the slices (Roberto et al. 2004a). The evoked IPSCs in CeA neurons from EtOH-dependent rats were significantly larger than in naïve rats. In EtOH-dependent rats, the mean baseline amplitude of mIPSCs was also significantly increased compared to naïve rats, suggesting a post synaptic effect of chronic EtOH (Roberto et al. 2004a). However, possible changes in the expression of GABAA receptor subunits were not characterized. It was also found that the baseline PPF ratio of IPSCs was
