Presynaptic ethanol effects at some synapses are secondary to release of neuromodulators that are themselves the direct mediators of increased vesicle fusion. The CeA, for example, expresses a number of neuropeptides (including corticotropin-releasing factor [CRF]) affected by ethanol, and peptides in this region are implicated in the processing of aversive stimuli and emotional salience. As such, CeA is critically involved in the negative affective states accompanying drug and alcohol abuse and addiction (Koob, 2015). CRF enhances GABAergic transmission in the CeA via presynaptic CRF1 receptors (Bajo et al., 2008; Cruz et al., 2012; Roberto et al., 2010). Acute ethanol also enhances this transmission (Kang-Park et al., 2013; Nie et al., 2004; Roberto et al., 2003; Roberto et al., 2004a), and this effect is CRF1 dependent, suggesting that ethanol acts indirectly to increase GABA release by facilitating local CRF release (Bajo et al., 2008; Nie et al., 2004) (Figure 2P). However, in some CeA neurons, the ethanol and CRF effects on GABA transmission are additive, suggesting distinct mechanisms of action. In the dorsolateral striatum, however, ethanol inhibits GABA release by enhancing
