Our finding that blocking dopaminergic systems resulted in lack of conditioned preference concurs with data from a large body of existing literature demonstrating the requirement for dopamine in reward. Despite extensive investigation on the role of dopamine in reward however, surprisingly little is known about the dopaminergic mechanisms mediating ethanol reward. In fact, much of the evidence investigating the role of dopamine in ethanol reward in mammals is conflicting. We speculate that much of the variation between results of these studies potentially derives from compensatory mechanisms that occur throughout development in mutant animals, and non-specific or ineffective pharmacological manipulations. The genetic tools available in Drosophila allow us to avoid these caveats by permitting precise temporal control over neurotransmission of dopaminergic cells. Our data is consistent with the findings that mice lacking the D2 receptor29 or DARPP-3230 show decreased CPP, and that both fluphenazine administration31 and dopamine receptor blockade32 prevent expression of memory for ethanol reward. This suggests a conserved role for dopamine in expression of conditioned preference in flies and mice.
