Neuronal nicotinic acetylcholine receptors (nAChRs) have recently been implicated in several human studies of nicotine-related behaviors (Amos et al., 2008; Berrettini et al., 2008; Bierut et al., 2007; Ehringer et al., 2007; Hung et al., 2008; Saccone et al., 2007; Schlaepfer et al., 2008a; Thorgeirsson et al., 2008; Zeiger et al., 2008) and they have been associated with alcohol dependence in the COGA sample as well (Wang et al., 2008). An emerging body of evidence suggests that nAChRs may be a common site of action for both nicotine and alcohol (Schlaepfer et al., 2008b). Several studies have shown that nAChRs are modulated by ethanol (Aistrup et al., 1999; Cardoso et al., 1999; Jerlhag et al., 2006). Furthermore, receptors containing the nAChR subunits β2 and/or β3 appear to be important to the dopamine-enhancing effects of ethanol, particularly those located in the ventral tegmental area (VTA) (Jerlhag et al., 2006). More recently, a partial nicotinic agonist known to affect both α4β2 containing receptors and α6β3 containing receptors, Varenicline, was shown to decrease voluntary ethanol consumption in rats (Steensland et al., 2007). Likewise,
