In addition to basic literature, reports in humans are also supportive of a compromised role of DA transmission in alcoholics. While alcohol increases DA release in healthy subjects (Boileau et al., 2003) with some gender differences (Urban et al., 2010), a reduced number of DA receptors has been observed (Volkow et al., 1996; Martinez et al., 2005) in alcoholics that appears to be accompanied by a blunted DA release (Martinez et al., 2005, 2007; Volkow et al., 2007). While the reduced number of DA receptors could be, at first sight, be viewed as suggesting an increased DA release, it should be noted that by administering the DA inhibitor alpha methyl-para-tyrosine, Martinez et al. (2009) were able to exclude this possibility. Indeed, while healthy controls do show an increased raclopride binding after acute alpha methyl-para-tyrosine administration, cocaine-dependent subjects do not (or to a significantly lesser extent; Martinez et al., 2009). Similar results were obtained with the dopamine releasing agent methylphenidate (Volkow et al., 2007) and amphetamine (Martinez et al., 2005) in alcoholics. Notably, artificially increasing the brain levels of DAD2 receptors,
