Naltrexone is used as pharmacotherapy for alcohol use disorder. Its mechanism for reducing craving and relapse is:
- A Inhibiting aldehyde dehydrogenase, creating an aversive reaction to alcohol
- B Blocking mu-opioid receptors, attenuating the rewarding and euphorigenic effects of alcohol on the mesolimbic dopamine system ✓
- C Enhancing GABA-A receptor function, reducing withdrawal symptoms
- D Partial agonism at dopamine D3 receptors, reducing cue-induced craving
Explanation
Naltrexone is an opioid receptor antagonist (predominantly mu, also kappa and delta). Alcohol stimulates the release of endogenous opioids (beta-endorphin), which then activate mu-opioid receptors in the ventral tegmental area and nucleus accumbens, increasing mesolimbic dopamine release and producing rewarding/euphoric effects. Naltrexone blocks this opioid-mediated dopamine reward, reducing alcohol-induced euphoria and craving. The COMBINE study demonstrated its efficacy in reducing heavy drinking days and increasing abstinence. Disulfiram (not naltrexone) inhibits ALDH (option A). Acamprosate modulates NMDA/GABA balance (not naltrexone).
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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