agonists and should attempt to discriminate CB1- versus CB2-mediated drug actions before ascribing a role to CB1. In addition to CB2, evidence from the past decade has indicated that the TRPV1 receptor is also associated with the EC system namely through activation by AEA, and several studies have demonstrated that ethanol potentiates TRPV1 mediated responses (Nicoletti et al., 2008; Trevisani et al., 2002; Vetter et al., 2008). More importantly, TRPV1 null mutant mice display higher ethanol preference and reduced sensitivity to ethanol induced sleep and ataxia, and the reduced behavioral sensitivity to ethanol are also observed in wt mice administered a TRPV1 antagonist (Hinson and Siegel, 1986). These results suggest that AEA signaling through TRPV1 may prove important to mediating some effects of EC signaling in response to ethanol, and future studies should examine alterations in TRPV1 expression and function following chronic ethanol treatment.
