Acamprosate (calcium acetyl homotaurinate) is used in alcohol use disorder relapse prevention. What is its primary mechanism of action?

• A Mu-opioid receptor antagonism reducing reward
• B Aldehyde dehydrogenase inhibition producing aversive reaction
• C Dopamine D2 receptor partial agonism reducing craving
• D Modulation of glutamate (NMDA) and GABA neurotransmission to reduce post-acute withdrawal hyperexcitability ✓

Explanation

Acamprosate (calcium acetyl homotaurinate) reduces post-acute withdrawal syndrome (PAWS) in alcohol use disorder by modulating glutamatergic neurotransmission (reducing hyperactive NMDA receptor activity that develops after chronic alcohol use) and potentially enhancing GABAergic inhibitory tone. Chronic alcohol use upregulates NMDA receptors; upon cessation, glutamate hyperactivity drives craving and dysphoria — acamprosate attenuates this. It is best started after detoxification and continued even in relapse (unlike disulfiram). Naltrexone acts via mu-opioid antagonism. Disulfiram inhibits aldehyde dehydrogenase. Acamprosate has no hepatic metabolism (renal excretion) — preferred in liver disease.

Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.

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