In light of the implication of endogenous opioids in alcohol-induced reward, several genetic association studies have focused on genetic variation in the mu opioid receptor (OPRM1) gene as a plausible candidate locus for alcoholism phenotypes. In particular, a single nucleotide polymorphism (SNP) of the OPRM1 gene, the A118G SNP (rs17799971), has received significant attention given molecular evidence that this locus is a site of glycosylation. This non-synonymous mutation results in an amino acid change from asparagine to aspartic acid, which in turn is thought to increase binding affinity for β-endorphin (Bond et al., 1998). An additional study has shown that this polymorphism affects gene expression (Zhang et al., 2005), yet the exact molecular mechanisms remain elusive. Genetic association studies have examined this polymorphism in relation to diagnostic phenotypes of alcohol and drug dependence with mixed results(Arias et al., 2006). However, an experimental study focusing on behavioral mechanisms of alcohol reward in a sample of heavy drinkers has shown that compared to A-allele homozygotes, G-allele carriers report greater subjective reinforcement from alcohol in the laboratory (Ray and Hutchison, 2004). Similar results
