social facilitation (Varlinskaya and Spear, 2009, 2010)] is associated with an individual’s propensity to abuse alcohol. Interestingly, there may be pharmacological validity for this behavioral phenotype, such that the histaminergic (c.f., Panula and Nuutinen, 2011 and references therein) and ghrelin (c.f., Jerlhag et al., 2011b and references therein) systems have been implicated in ethanol-induced motor activation, ethanol-induced conditioned place preference, alcohol-preference and high alcohol consumption behavior. However, the positive relationship between ethanol-induced motor stimulation and high ethanol intake does not always hold. For example, low alcohol-consuming DBA/2J mice display greater acute ethanol-induced motor stimulation than high alcohol-consuming C57BL/6J mice (e.g., Melon and Boehm, 2011). Moreover, there are concerns with establishing consilience and translatability of ethanol-induced stimulation between the rodent and clinical literature (c.f., Crabbe et al., 2010). For instance, rodents can only provide a rudimentary model of the cognitive constructs associated with human approach behavior, aggression and social facilitation. In addition, other than low- to moderate-dose effects on self-report (Morzorati et al., 2002; Viken et al., 2003), heart rate (Finn and Justus, 1997; Peterson et al., 1996), and brain activity (Lukas et al., 1986; Sorbel et al., 1996; Trim et al., 2010) the stimulating effects of ethanol are not as
