The activity of mesolimbic DA neurons in the VTA is closely associated with the reward and learning processes thought to drive the transition to compulsive drug use (Morikawa and Morrisett, 2010), and one of the major targets for these neurons is the NAc. Along these lines, Cheer et al (2004) reported that acute administration of WIN enhanced the frequency of fast, spontaneous DA transients in the NAc of freely moving rats. In a subsequent study, they found that acute ethanol administration also increased DA release in the NAc, and this effect could be blocked by pre-treating the rats with SR, suggesting that CB1 function was required for the ethanol-mediated activation of VTA DA neurons (Cheer et al., 2007). As mentioned in the previous section, similar results have also been obtained from single-unit recordings of VTA DA neurons where pre-treatment with SR blocks the increased firing rate observed after acute ethanol administration (Perra et al., 2005). Consistent with these findings, CB1 KO mice lack the increase in NAc DA concentrations observed in wt mice following an acute injection of ethanol (Hungund
