Chronic ethanol exposure and intake also alter GABAergic transmission via pre- and postsynaptic mechanisms. These effects were covered in a recent review (Roberto and Varodayan, 2017) and will not be discussed in detail here. Both increases and decreases in GABA release are observed in several brain regions and they appear to be synapse specific (Cuzon Carlson et al., 2011; Herman et al., 2016a; Schindler et al., 2016; Tremwel et al., 1994; Wanat et al., 2009; Wilcox et al., 2014) (Figures 3E–3G). In the CeA, for example, CRF levels and GABA transmission are increased and remain so during acute withdrawal. Interestingly, acute ethanol exposure following chronic ethanol treatment has the same effect as acute ethanol in naive animals, suggesting that acute ethanol-induced facilitation of GABA transmission does not undergo tolerance (Roberto et al., 2004a) (Figure 3G).
