Since it has been speculated that dopamine tone/release might underlie the stimulant response to alcohol observed in heavy drinkers (King et al., 2002) and early stage alcoholics (Thomas et al., 2004) and since naltrexone reduces ventral striatal dopamine output in rodents (Gonzales and Weiss, 1998) and also reduces alcohol-induced stimulation in man (Anton et al., 2004; Ray and Hutchison, 2007) it is conceivable that there might be a salient interaction between the opiate and dopamine systems that might be genetically based and modified by naltrexone. For instance, DAT 9-repeat carriers might be more likely to have elevated dopamine levels in nucleus accumbens after alcohol consumption or cue-presentation and therefore be more likely to respond to naltrexone - secondary to its ability to decrease alcohol or cue-induced dopamine release.
