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 VTA are mediated by α3β2* and/or β3*, rather than α4β2*, α7, or α6* nAChRs; however, it remains unclear if these effects are due to direct or indirect interactions of ethanol with nAChRs.
