Ethanol has well-known locomotor and reinforcing effects, and certainly the latter contribute to drinking in some capacity. Thus, top-down approaches based on these behavioral outcomes led scientists to study ethanol’s effects on midbrain dopamine neurons that have prominent roles in locomotion and reward (Melis et al., 2007; Samson et al., 1992). Although findings suggest that lesions of the mesolimbic dopamine system do not change ethanol self-administration (Rassnick et al., 1993), rodents do self-administer ethanol into the VTA (Gatto et al., 1994; Rodd et al., 2004), and dopamine is clearly implicated in ethanol-induced increases in locomotion and sensitization (Phillips and Shen, 1996). Ethanol facilitates action potential firing of midbrain dopamine neurons (Figure 2A) and increases extracellular dopamine levels in the VTA (Deehan et al., 2016) (Figure 2C). The physiological mechanisms thought to underlie this ethanol potentiation were reviewed by Morikawa and Mornsett (2010) and include reductions of a barium-sensitive potassium and M-type currents. Furthermore, GIRK channels (Herman et al., 2015) and the hyperpolarization-activated and cyclic nucleotide-gated (HCN) channel current (Ih) (Appel et al., 2003; McDaid et al., 2008; Nimitvilai et al.,
