Additional data from Roberto et al. (2004a, 2010) further suggest that chronic EtOH exposure can affect CeA GABA release, perhaps via an action on GABAergic terminals. Baseline GABAA IPSCs were significantly higher, and baseline PPF of GABAA IPSCs was significantly smaller in CeA neurons from EtOH-dependent rats compared to non-dependent rats, suggesting that evoked GABA release was augmented after chronic EtOH exposure. These investigators also reported an increase in the baseline frequency of mIPSCs in CeA neurons from EtOH-dependent rats compared to that of naïve controls. Acute superfusion of EtOH significantly enhanced GABAA IPSCs, decreased the PPF ratio of IPSCs, and increased the mIPSC frequency to the same extent in CeA slices from EtOH-dependent rats and naïve rats, suggesting a lack of tolerance to the presynaptic acute EtOH effects (Roberto et al. 2004a). In addition, these investigators estimated the interstitial GABA levels in CeA using microdialysis in freely moving rats. In agreement with the in vitro electrophysiologic results, the in vivo data showed a fourfold increase of baseline dialysate GABA concentrations in CeA of EtOH-dependent rats compared to naïve rats.
