naltrexone. It has been shown that some of this enhanced alcohol response and drinking behavior in rodents engineered to have a homologous SNP is due to increased dopamine release in the nucleus accumbens (Ramchandani et al., 2011) which in general is thought to be a signature of reinforcement and addiction. Of interest, naltrexone has been shown in animals to both reduce nucleus accumbens dopamine release (Gonzales and Weiss, 1998) and to reduce drinking in rodent (Middaugh and Bandy, 2000) and non-human primate drinking models (Kornet et al., 1991). Of great interest, an homologous SNP to that found in humans in the mu opioid receptor gene occurring naturally in non-human primates also appears to confer both sensitivity to alcohol response (Barr et al., 2007) and response to naltrexone in the reduction of alcohol effects and consumption (Barr et al., 2010; Vallender et al., 2010). This finding parallels data in human clinical lab studies (Ray et al., 2011) and clinical trials (Oslin et al., 2003; Anton et al., 2008) where naltrexone appears to exert a stronger effect on those individuals with the asp40 OPRM1 SNP. However, this finding is not universal as several reports suggest that it may not be as salient
