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Pharmacological Mechanisms of Naltrexone and Acamprosate in the Prevention of Relapse in Alcohol Dependence
Author(s) -
Littleton John,
Zieglgänsberger Walter
Publication year - 2003
Publication title -
the american journal on addictions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.997
H-Index - 76
eISSN - 1521-0391
pISSN - 1055-0496
DOI - 10.1111/j.1521-0391.2003.tb00492.x
Subject(s) - naltrexone , acamprosate , glutamatergic , relapse prevention , alcohol dependence , endogenous opioid , glutamate receptor , psychology , pharmacology , addiction , antagonist , neuroscience , alcohol , opioid , medicine , psychiatry , receptor , chemistry , biochemistry
Naltrexone and acamprosate may ultimately prove to be useful additions to pharmacotherapy for alcoholism by reducing relapse. Naltrexone is a relatively selective competitive antagonist at mu‐opioid receptors, and this activity may explain its anti‐relapse action either because endogenous opioids are involved in the positively reinforcing effects of alcohol and/or because these same transmitters are involved in the conditioned anticipation of these effects. In contrast, the pharmacology of acamprosate is still poorly understood. This is not surprising because it is a small flexible molecule with similarities to several neuro‐active amino acids and is used in high doses. All these factors suggest that it may have multiple actions. Currently, the best explanation for the effects of acamprosate seems to be that it inhibits the glutamatergic transmitter system involved in both the negative reinforcing effects of alcohol and the conditioned “pseudo‐withdrawal” that may be important in cue‐induced relapse.