Ethanol affects multiple signaling pathways in the brain, including dopamine (DA) (Theile et al., 2011; Ben Hamida et al., 2012; Li et al., 2012), serotonin (Engel and Allan, 1999; Sung et al., 2000; McBride et al., 2004; Rodd et al., 2010), opioids (Marinelli et al., 2010; Walker et al., 2011), corticosteroids (Vendruscolo et al., 2012), adenosine (Nam et al., 2013), and galanin (Lewis et al., 2004) pathways. Originally, ethanol was hypothesized to interact non-specifically with membrane lipids and consequently, alter the function of integral membrane proteins like ion channels (Harris et al., 2008; Howard et al., 2011b). Indeed, ethanol can modify the activity of some lipid kinases (Tong and Sun, 1996). More recently, it has become clear that ethanol can also modulate ion channels through distinct alcohol binding pockets in the channel protein (Harris et al., 2008; Howard et al., 2011b). Alcohol has been reported to affect several ion channels in the brain. For example, ethanol modulates GABAA (Mihic et al., 1994) glycine receptors (Mihic et al., 1997), Ca2+-dependent K+ channels (Dopico et al., 1998), and acetylcholine receptors (Cardoso et
