To date, most studies involving the role of the EC system in AUDs have focused on EC transmitters, their related synthetic and inactivating enzymes, and the CB1 receptor. This is almost certainly due to the well-ingrained dogma in the cannabinoid field that CB1 represents the central cannabinoid receptor (Matsuda et al., 1990) and CB2 is the peripheral cannabinoid receptor (Bayewitch et al., 1995). However, the existence and role of central CB2 receptors is beginning to gain some traction (Atwood and Mackie, 2010; Onaivi et al., 2011), and a recent behavioral study indicates that CB2 is involved anxiogenic, pneumonic, and motoric processes (Ortega-Alvaro et al., 2011). Furthermore, ethanol treatment and consumption is known to alter CB2 gene expression in the brain (Onaivi et al., 2008). As a consequence, future research should be mindful of the lack of specificity of most cannabinoid 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
