Naltrexone reduces alcohol craving and relapse primarily through which mechanism?
- A Blocking the aversive taste of alcohol via gustatory pathways
- B GABA-A potentiation reducing alcohol withdrawal severity
- C Blocking mu-opioid receptors, thereby attenuating the dopamine-mediated reward ('high') of alcohol in the mesolimbic pathway ✓
- D NMDA receptor antagonism reducing glutamate-mediated craving
Explanation
Alcohol induces release of endogenous opioids (beta-endorphin) which activate mu-opioid receptors, stimulating mesolimbic dopamine release and producing the reinforcing 'high'. Naltrexone, a mu/kappa/delta opioid receptor antagonist, blocks this opioid-mediated dopamine reward, reducing the pleasurable effect of alcohol and thereby decreasing craving and relapse. Acamprosate acts via NMDA/GABA mechanisms to reduce protracted abstinence syndrome craving. GABA modulation is relevant to benzodiazepines used in detoxification, not naltrexone.
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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