{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,11]],"date-time":"2025-09-11T06:07:52Z","timestamp":1757570872375,"version":"3.35.0"},"reference-count":33,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2008,1,22]],"date-time":"2008-01-22T00:00:00Z","timestamp":1200960000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2008,2]]},"abstract":"<jats:p><jats:bold>Background:\u2002<\/jats:bold>Acamprosate (calcium acetylhomotaurinate) has proven to be a moderately effective pharmacological adjunct for the treatment of alcoholism. However, the central nervous system mechanism by which acamprosate reduces alcohol relapse remains unclear. Here we survey a number of metabotropic receptors, ligand\u2010gated ion channels, and voltage\u2010gated ion channels, to determine if acamprosate has actions at these sites in the central nervous system.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold><jats:italic>Xenopus<\/jats:italic>oocytes were injected with cDNAs or cRNAs encoding metabotropic glutamate receptors 1 and 5, M1 muscarinic receptors, glycine \u03b11 homomeric and \u03b11\u03b21 heteromeric receptors, \u03b3\u2010aminobutyric acid A (GABA<jats:sub>A<\/jats:sub>\u03b14\u03b23\u03b4, \u03b14\u03b23\u03b32s, and \u03b11\u03b22\u03b32s) receptors, vanilloid receptor 1, and various combinations of \u03b1 and \u03b2 subunits of voltage\u2010gated Na<jats:sup>+<\/jats:sup>channels. Electrophysiological responses were measured using two\u2010electrode voltage clamp parameters after activation with agonists or voltage steps (for the voltage\u2010gated channels). Acamprosate (0.1 to 100\u2003<jats:italic>\u03bc<\/jats:italic>M) was pre\u2010applied for 1\u2003minute, followed by co\u2010application with agonist. Acamprosate was also applied with ethanol to determine if it altered ethanol responses at some of these receptors and channels.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold>None of the receptors or ion channels responded to acamprosate alone. Acamprosate also failed to alter the activation of receptors or channels by agonists or after activation of voltage\u2010gated channels. There was no effect of acamprosate on ethanol responses at GABA<jats:sub>A<\/jats:sub>\u03b11\u03b22\u03b32s receptors or Na<jats:sup>+<\/jats:sup>channels.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold>Acamprosate does not significantly modulate the function of these receptors and ion channels at clinically relevant concentrations. Thus, the clinical effectiveness of acamprosate in the treatment of alcoholism is not likely due to direct effects on these receptors or ion channels.<\/jats:p>","DOI":"10.1111\/j.1530-0277.2007.00569.x","type":"journal-article","created":{"date-parts":[[2008,9,17]],"date-time":"2008-09-17T12:36:10Z","timestamp":1221654970000},"page":"188-196","source":"Crossref","is-referenced-by-count":25,"title":["Effects of Acamprosate on Neuronal Receptors and Ion Channels Expressed in<i>Xenopus<\/i>Oocytes"],"prefix":"10.1111","volume":"32","author":[{"given":"Matthew T.","family":"Reilly","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ingrid A.","family":"Lobo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lindsay M.","family":"McCracken","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cecilia 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