evidence for the use of DA agonists as a treatment for alcohol and/or substance use disorders is inconclusive (Swift, 2010), there has been a revived interest for these drugs, possibly because adequate neurobiological rationale (Melis et al., 2005) is now available. For example, aripiprazole (Semba et al., 1995; Burris et al., 2002; Shapiro et al., 2003) a partial DA agonist which in principle should antagonize DA when tone is high, whereas should increase DA transmission when basic tone is low, represents a proposed treatment for alcohol abuse disorders (Kenna et al., 2009). Human laboratory alcohol studies have shown that aripiprazole reduces drinking (Kranzler et al., 2008), especially in the more impulsive alcoholic (Voronin et al., 2008). An fMRI study demonstrated that aripiprazole significantly attenuates neural activity in the ventral striatum in response to alcohol cues (Myrick et al., 2010) thereby suggesting a therapeutic potential for cue-induced relapse. Further, a 12-week, double-blind, placebo-controlled treatment study with 295 alcohol-dependent individuals found that aripiprazole initially decreased heavy drinking days compared to placebo, but this significant effect was not present when the target dose of 30 mg was reached (Anton et al., 2008). This trial also showed greater side-effects and greater study discontinuation in
