One of the key neurotransmitter systems associated with alcohol-induced reward is the endogenous opioid system. It is known that alcohol consumption leads to an increase of endogenous opioids, β-endorphin in particular (Marinelli et al., 2003), which is linked to reinforcement after alcohol consumption. The binding of β-endorphin to µ-opioid receptors may reinforce alcohol drinking directly or indirectly through increased dopamine levels in the brain reward areas (Gianoulakis, 2009). Genetic variation in the μ-opioid receptor may hence affect the risk of developing alcohol use disorder by affecting the individual's response to alcohol. This hypothesis is supported by animal studies: e.g. mice lacking the μ-opioid receptor self-administer less alcohol than wild type mice (Roberts et al., 2000; Hall et al., 2001). Furthermore, opioid receptor antagonists such as naltrexone and naloxone reduce alcohol self-administration in animal studies, and in human studies they have been effective in preventing relapse to heavy drinking and in reducing craving for alcohol (reviewed, e.g. by Sinclair, 2001; Bouza et al., 2004; Thorsell, 2013). Taken together, accumulating evidence implicates human µ-opioid receptor as an important determinant in the reinforcing
