Lack of effects of Ca-acetyl homotaurinate on chronic and acute toxicities of ethanol in rats

Magnen, J. Le; Tran, Giang N.; Durlach, J

doi:10.1016/0741-8329(87)90006-1

Cited by 41 publications

(12 citation statements)

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“…Acamprosate produces a dose-dependent reduction in voluntary alcohol intake in animals with no effect on food and water consumption. There is no evidence of pharmacological interactions with ethanol or other compounds used in alcoholism treatment (anxiolytics, hypnotics, disulfiram) [3,7,10,16,34]. It has no other pharmaceutical effects than reducing alcohol intake (e.g.…”

Section: Biological Basis For the Acamprosate Studiesmentioning

confidence: 96%

The European acamprosate trials: Conclusions for research and therapy

et al. 2001

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In an excellent methodological approach, the European acamprosate study project showed that acamprosate increases sobriety times. In one randomized prospective study (n = 260) comparing acamprosate and placebo, with a 1-year treatment phase and 1-year follow-up phase, the authors found that acamprosate is effective only in Lesch type I and type II patients. To investigate the possible influence of diagnostic subgrouping, we applied the Lesch typology in a co-work with the main researchers of the UK study. The UK results concerning acamprosate's effects in the types do not mirror the Vienna results, but the numbers of type I and type II patients, retrospectively found as included in the UK centers, were too small for any conclusions. The distribution of the types points to the fact that too many type III and IV patients had been included to give acamprosate the chance to be effective. Following our typology and also these studies, we developed special treatment approaches. For relapse prevention studies, the cumulative abstinence duration together with the Lesch typology seems to be promising.

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Section: Biological Basis For the Acamprosate Studiesmentioning

confidence: 96%

The European acamprosate trials: Conclusions for research and therapy

et al. 2001

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“…Acamprosate attenuates: a) ethanol consumption in rodents without affecting water intake (Boismare et al 1984;Le Magnen et al 1987); b) suppresses conditioned cue responses to ethanol in previ-330 Fig. 2 Schematic representation of acamprosate's effects.…”

Section: Nmda Antagonistsmentioning

confidence: 98%

Neuropharmacological treatments for alcoholism: scientific basis and clinical findings

Johnson¹,

Ait-Daoud

2000

Psychopharmacology

159

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Preclinical studies have exploded our knowledge about the behavioral and biological underpinnings of alcoholism. These studies suggest that certain neurotransmitters, particularly those interacting with the opioid, N-methyl-D-aspartate, and monoamine systems, may play a critical role in the expression of alcohol-drinking and other behaviors associated with its abuse liability. Built upon this foundation, important advances have been made in the development of therapeutic medications for the treatment of alcoholism. Of the medications reviewed, acamprosate's potential appears to be the most widely established. In the USA, naltrexone was approved by the Food and Drug Administration in 1995 for the treatment of alcoholism; however, the results of some studies have been less encouraging. Naltrexone's reliance on high compliance rates for efficacy may, eventually, limit its potential in clinical settings offering generic treatment for alcoholism. The relative paucity of dose-response studies on naltrexone's effects in treating alcoholics is an important gap in the literature. Recent data from a large clinical trial suggests that ondansetron, a serotonin3 antagonist, offers new hope for the treatment of early onset alcoholics; a type of alcoholism most difficult to manage with psychosocial measures alone. Different subtypes of alcoholic may, therefore, have varying treatment responses to serotonergic agents. Matching subtypes of alcoholic to effective treatment medications based upon their different biologies remains an important therapeutic goal. Combinations of effective pharmacological agents need exploration as they may prove to be synergistic, and could shepherd in a new era of treatments aimed at multiple neurotransmitter targets associated with the alcoholism disease. The coming decade promises more powerful tools for characterizing drug effects on alcohol drinking, thereby closing the gap between animal models of addiction and the human condition.

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“…Evidence that acamprosate modulates a novel site of action at mGluR5 comes from the finding that it inhibits the binding and neurotoxic effects of ±-1-aminocyclopentane-trans-1,3-dicarboxylic acid [86]. Acamprosate has been shown to decrease: a) ethanol consumption in rodents [87][88][89], but this effect may not be specific in food-deprived C57BL/6J mice as both ethanol and water were reduced in a schedule-induced polydipsia task [90]; b) dopamine hyperexcitability in the nucleus accumbens during alcohol withdrawal [91,92]; c) general neuronal hyperexcitability [93,94]; d) glutamatergic neurotransmission in alcohol-dependent rats [91,95]; e) voltage-gated calcium channel activity, and f) the expression of brain c-fos, an immediate early gene associated with alcohol withdrawal [96,97]. Nevertheless, it is acamprosate's ability to suppress alcoholinduced glutamate receptor sensitivity [98], as well as conditioned cue responses to ethanol in previously dependent animals even after prolonged abstinence [99][100][101][102], that has been linked with its therapeutic effect in humans -dampening negative affect and craving post-abstinence [14,103] (Fig.…”

Section: Glutamate Metabotropic Glutamate Receptor-5 (Mglur5) Modulatmentioning

confidence: 99%

Update on neuropharmacological treatments for alcoholism: Scientific basis and clinical findings

Johnson

2008

Biochemical Pharmacology

237

182

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The past decade has seen an expansion of research and knowledge on pharmacotherapy for the treatment of alcohol dependence. The Food and Drug Administration (FDA)-approved medications naltrexone and acamprosate have shown mixed results in clinical trials. Oral naltrexone and naltrexone depot formulations have generally demonstrated efficacy at treating alcohol dependence, but their treatment effect size is small, and more research is needed to compare the effects of different doses on drinking outcome. Acamprosate has demonstrated efficacy for treating alcohol dependence in European trials, but with a small effect size. In U.S. trials, acamprosate has not proved to be efficacious. Research continues to explore which types of alcohol-dependent individual would benefit the most from treatment with naltrexone or acamprosate. The combination of the two medications demonstrated efficacy for treating alcohol dependence in one European study but not in a multi-site U.S. study. Another FDA-approved medication, disulfiram, is an aversive agent that does not diminish craving for alcohol. Disulfiram is most effective when given to those who are highly compliant or who are receiving their medication under supervision. Of the non-approved medications, topiramate is among the most promising, with a medium effect size in clinical trials. Another promising medication, baclofen, has shown efficacy in small trials. Serotonergic agents such as selective serotonin reuptake inhibitors and the serotonin-3 receptor antagonist, ondansetron, appear to be efficacious only among certain genetic subtypes of alcoholic. As neuroscientific research progresses, other promising medications, as well as medication combinations, for treating alcohol dependence continue to be explored.

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Lack of effects of Ca-acetyl homotaurinate on chronic and acute toxicities of ethanol in rats

Cited by 41 publications

References 9 publications

The European acamprosate trials: Conclusions for research and therapy

The European acamprosate trials: Conclusions for research and therapy

Neuropharmacological treatments for alcoholism: scientific basis and clinical findings

Update on neuropharmacological treatments for alcoholism: Scientific basis and clinical findings

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