Ethanol increases the firing rate of dopaminergic neurons, especially the “tonic” firing exhibited by these continuously-active neurons (Mereu, Fadda et al. 1984, Gessa, Muntoni et al. 1985). This effect is best known to occur in the limbic VTA, but in fact ethanol also enhances firing of SNc dopaminergic neurons. The molecular targets of ethanol that produce this effect are still not fully characterized (Melis, Diana et al. 2009, Morikawa and Morrisett 2010). It does seem clear that this increase in firing underlies the increase in extracellular dopamine observed in the striatum (including dorsal striatum) following ethanol exposure in vivo (Yim, Schallert et al. 1998, Gonzales, Job et al. 2004). Ethanol-induced increases in DA and activation of dopamine receptors have been postulated to contribute to the rewarding effects of the drug, as well as locomotor activation and sensitization produced by ethanol at some doses in some mammalian species (Milton, Randall et al. 1995, Shen, Crabbe et al. 1995, Gonzales, Job et al. 2004, Abrahao, Quadros et al. 2012). However, increased DA could also contribute to the reinforcing effects of ethanol that