Although medications that increase DA activity could be effective in treating alcohol abuse disorders, conflicting results have been produced (Swift, 2010). For example, it was suggested that the DA agonist bromocriptine reduced drinking in alcoholics (Lawford et al., 1995), but a randomized, double-blind, placebo-controlled study using a long-acting injectable bromocriptine preparation in 366 alcoholic-dependent individuals did not find difference in alcohol relapse between medication and placebo (Naranjo et al., 1997). Another example is the stimulant medication modafinil (DA indirect agonist), found to improve cognition in 40 alcoholics with organic brain syndrome, but effects on drinking could not be measured (Saletu et al., 1990). However, modafinil reduced cocaine use in a placebo-controlled study with 62 cocaine-dependent individuals (Dackis and O’Brien, 2005), while another trial did not find differences between modafinil and placebo tested for methamphetamine users (Shearer et al., 2010). While 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
