In addition, acute EtOH (44 mM) increased IPSCs, decreased the PPF ratio of IPSCs and increased the mIPSCs frequency to the same extent in EtOH-dependent rats and naïve rats, suggesting a lack of tolerance for the acute EtOH effects (Roberto et al. 2004a). One of the most consistent findings from these recent studies is the lack of tolerance for the acute potentiating effect of EtOH on GABAergic synapses. These studies suggest that GABAergic mechanisms may not be associated with the tolerance that is known to develop with some of the behavioral effects of EtOH (e.g. ataxia, sedation). Additional studies will be needed to more carefully determine the molecular mechanisms responsible for these adaptive changes in different brain regions and length/duration of EtOH exposure required to induce such neuroadaptations in GABAergic synapse. Moreover, these data also suggest that, as with the acute effects of EtOH, long-term exposure to EtOH results in both pre and postsynaptic alterations and these changes may differ between brain regions (Siggins et al. 2005; Weiner and Valenzuela 2006).
