Alcohol has a complex pharmacological profile involving affinity for multiple receptor types; the reinforcing effects are thought to be due to the combined release of endogenous opioids like β-endorphin and dopamine (from the midbrain), targeting neurons in the nucleus accumbens (NAc) downstream (Gianoulakis et al., 1996, Volpicelli, 2001). Current models of the effects of naltrexone posit that it acts by diminishing the dopamine response to ethanol in the NAc, which has been supported by pre-clinical research (Benjamin et al., 1993). Human laboratory studies have demonstrated that naltrexone dampens alcohol-induced feelings of stimulation (Drobes et al., 2004, Swift et al., 1994), decreases liking of alcohol (McCaul et al., 2001), and increases alcohol-induced fatigue and confusion (King et al., 1997).
