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Biology Articles » Neurobiology » Neurobiology of Diseases & Aging » Neurobiology of addiction and implications for treatment » Alcohol Withdrawal: the role of glutamate

Alcohol Withdrawal: the role of glutamate
- Neurobiology of addiction and implications for treatment

The neurobiology of alcoholism involves many different neurotransmitters, but key are the gamma-aminobutyric acid (GABA)-ergic system and the glutamatergic system (Nutt, 1999). In alcohol withdrawal, increased glutamatergic NMDA function is present and is thought to be involved in seizures and cell death, by means of increased Ca2+ influx through its channel and low Mg2+. The hippocampus appears to be a critical site for such glutamatergic hyperactivity. Acamprosate, a taurine derivative, is increasingly used to maintain abstinence from alcohol as it has been shown to double abstinence rates. How acamprosate achieves its therapeutic effect has not yet been fully characterised; it antagonises the NMDA receptor (possibly through the polyamine site). Acamprosate also reduces glutamate levels and may be neuroprotective (Dahchour & De Witte, 2000). If such neuroprotection occurs in humans, this would have important implications for the treatment of alcoholism; currently some workers advocate starting acamprosate with detoxification.


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