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. Moreover, local administration of EtOH by dialysis increased the dialysate GABA levels in CET rats. These findings again indicate a lack of tolerance to presynaptic acute EtOH effects on GABA release in CeA of CET rats (Roberto et al. 2004a). These studies strengthen the possibility that chronic as well as acute EtOH may alter the function of the GABAergic synapses acting at both the postsynaptic site and presynaptic terminals. Altogether, these data suggest that long-term exposure to EtOH causes changes at GABAergic synapses that may differ between brain regions and with the duration of chronic exposure. Further studies will be needed to more carefully determine the specific exposure durations required to elicit these changes in GABAergic synapses, the molecular mechanisms responsible for these adaptive changes, as well as their behavioral consequences with respect to withdrawal and dependence.
