Impulsivity and Drinking /Craving: Effect of a Dopamine Stabilizer Medication
Principal Investigator: Raymond Anton, M.D.
Co-Principal Investigator: Hugh Myrick, M.D.
Co-Investigator: Konstantin Voronin, M.D., Ph.D.
In this research component, individual “trait-impulsivity” differences that might predict a risk for the development of alcohol dependence and/or risk for relapse have been identified and are being further investigated.
Findings in animals and humans suggest that a dysfunctional brain dopamine system underlies impulsive traits. Given that the dopamine system underlies both impulsivity and reward areas in the brain, it is not surprising that individuals high in trait-impulsivity show different brain regional activity to reward than individuals low in trait-impulsivity. Interestingly, these areas of activation in the brain are similar to what has been observed in non-treatment seeking alcoholics (NTSA) following the presentation of alcohol cues. We found that aripiprazole, a drug that is thought to “stabilize” the dopamine system, reduces drinking and blocks alcohol cue-induced activity in the ventral striatal area of the brain in NTSAs, and it does so most clearly in individuals with high trait-impulsivity.
The aim of this component is to replicate and extend this original finding with aripiprazole, in a medication group by trait-impulsivity group experimental design. In addition to studying the interaction of aripiprazole and trait-impulsivity, we will also systematically evaluate the role of trait-impulsivity and aripiprazole, per se, as main effects on drinking and craving using our well-validated, natural drinking, brain imaging, and other consumption paradigms. Finally, we will explore whether functional genetic variants in the brain dopamine system might underlie trait-impulsivity effects and/or aripiprazole response.