A patient recovering from alcohol dependence is started on acamprosate. Its mechanism of action for reducing cravings is:
- A Blocking mu-opioid receptors to reduce alcohol reward
- B Inhibiting aldehyde dehydrogenase to produce an aversive reaction to alcohol
- C Partial agonism at GABA-B receptors, reducing withdrawal anxiety
- D Modulating NMDA glutamate receptors (antagonism) and GABA-A receptors (positive modulation) to normalise chronic alcohol-induced glutamatergic hyperexcitability ✓
Explanation
Acamprosate (calcium acetyl homotaurinate) is thought to modulate the neurochemical imbalance created by chronic alcohol use during abstinence. Chronic alcohol suppresses NMDA-mediated glutamatergic activity; upon cessation, compensatory NMDA receptor upregulation creates a state of glutamatergic hyperexcitability that manifests as anxiety, dysphoria, and craving. Acamprosate is believed to act as a functional NMDA antagonist and/or GABA-A positive modulator, restoring the glutamate/GABA balance and reducing protracted withdrawal symptoms and craving. It has no aversive or rewarding properties and is most effective in patients who are already abstinent at initiation.
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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