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The mechanism of action of acamprosate has been less clear, but in the decade or more that has elapsed since its licensing, a body of translational evidence has accumulated, in which preclinical findings are replicated in clinical populations. Acamprosate modulates <jats:italic><jats:styled-content style=\"fixed-case\">N<\/jats:styled-content><\/jats:italic>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010aspartic acid receptor transmission and may have indirect effects on \u03b3\u2010aminobutyric acid type <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> receptor transmission. It is known to decrease brain glutamate and increase \u03b2\u2010endorphins in rodents and man. Acamprosate diminishes reinstatement in ethanolized rodents and promotes abstinence in humans. Although acamprosate has been called an anticraving drug, its subjective effects are subtle and relate to diminished arousal, anxiety and insomnia, which parallel preclinical findings of decreased withdrawal symptoms in animals treated with acamprosate. Further understanding of the pharmacology of acamprosate will allow appropriate targeting of therapy in individuals with alcohol dependence and extension of its use to other addictions.<\/jats:p>","DOI":"10.1111\/bcp.12070","type":"journal-article","created":{"date-parts":[[2012,12,25]],"date-time":"2012-12-25T11:29:43Z","timestamp":1356434983000},"page":"315-323","source":"Crossref","is-referenced-by-count":116,"title":["The clinical pharmacology of acamprosate"],"prefix":"10.1111","volume":"77","author":[{"given":"Nicola J.","family":"Kalk","sequence":"first","affiliation":[{"name":"Centre for Neuropsychopharmacology Imperial College London  London W12\u20090NN UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne R.","family":"Lingford\u2010Hughes","sequence":"additional","affiliation":[{"name":"Centre for Neuropsychopharmacology Imperial College London  London W12\u20090NN 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