The effects of increased AEA on ethanol consumption are likely mediated by activation of the CB1 receptor as numerous studies have demonstrated that direct modulation of CB1 alters ethanol intake. Studies utilizing CB1 agonists to modulate ethanol consumption are confronted with the potential confound that CB1-mediated reductions in motor activity may act synergistically with those of ethanol thereby occluding any enhancement in the motivation to consume ethanol. In keeping with this effect, two studies have reported that decreased ethanol consumption and self-administration following systemic injection of WIN is correlated with reduced locomotor activity (Cippitelli et al., 2007; Linsenbardt and Boehm, 2009). In addition, CB1 agonists are known to induce hyperphagia that may confound studies examining ethanol preference where sweetened or otherwise flavored solutions are used as controls (Dewey, 1986). However, Gallate et al (1999) concluded that pre-treatment with a CB1 agonist increased the motivation of rats to self-administer beer despite increased responding for both control substances (near beer and sucrose) used in this study. More convincing results for the role of CB1 activation in the reinforcing properties of ethanol have
