While, it is relatively clear that α4β2* and α7 nAChRs play a major role for nicotine mediated dopamine effects in the VTA, it has been more difficult to determine the specific nAChR compositions important for ethanol. Several subunit-specific antagonists have been administered to mice both systemically and by direct infusion into the brain. Ethanol-induced DA release in the NAc and locomotor activity were blocked by systemic injections of MEC but not by methyllycaconitine citrate (MLA, α7 antagonist) or dihydro-β-erythroidine (DHβE, broad-spectrum β2*-antagonist), suggesting ethanol's stimulatory effects may not be mediated by β2*-containing or α7 nAChRs (Larsson et al., 2002). Another study further defined which subunits were involved in ethanol's effects on the DAergic system by administering various α-conotoxins into the VTA and measuring DA outflow in the NAc following an ethanol challenge. Results showed that α-conotoxin MII, selective for α3β2* and/or β3* and/or α6* subunits, significantly reduced ethanol-stimulated DA release in the NAc, while the selective α6* antagonist, α-conotoxin PIA-analog, showed no effect (Larsson and Engel, 2004; Jerlhag et al., 2006). Taken together, this evidence suggests ethanol's actions in the
