mechanism that likely contributes to this effect is a disinhibition of DA neurons produced by a CB1-mediated decrease of GABA release onto these neurons (Riegel and Lupica, 2004). In addition, acute ethanol inhibits hippocampal neurons via an EC-mediated reduction in glutamate release (Basavarajappa et al., 2008). If this can be extended to cortical neurons then ethanol-mediated EC release would be expected to reduce cortical output thus producing a synergistic mechanism with the increased activity of the mesolimbic DA pathway. Alternatively, the effect of SR to reduce the activation of mesolimbic DA pathways could be due to an enhancement of mesocortical DA function in the presence of this compound (Tzavara et al., 2003), but numerous studies have reported that ethanol increases tissue content of ECs. For instance, Caillé et al (2007) reported increased 2-AG levels in the NAc of rats engaged in ethanol self-administration, and infusion of CB1 agonists into the posterior VTA facilitates ethanol consumption suggesting a common mechanism (Linsenbardt and Boehm, 2009). To clarify this point, future studies should seek to directly measure interstitial EC concentrations in the VTA following acute ethanol administration. However, the present data suggest that EC release from mesolimbic DA neurons in response to ethanol
