Abstract
The present paper summarizes the results of a number of pharmacological studies implicating the cannabinoid CB1 receptor in the neural circuitry regulating different alcohol-related behaviors in rodents. Specifically, cannabinoid CB1 receptor antagonists - including the prototype, rimonabant - have been reported to suppress: (a) acquisition and maintenance of alcohol drinking behavior under the 2-bottle “alcohol vs water” choice regimen; (b) the increase in alcohol intake occurring after a period of alcohol abstinence (an experimental model of alcohol relapse); (c) alcohols reinforcing and motivational properties measured in rats trained to perform a specific task (e.g., lever-pressing) to access alcohol; (d) reinstatement of extinguished alcohol-seeking behavior triggered in rats by a nicotine challenge or presentation of cues previously associated to alcohol availability (another model of alcohol relapse). Additional data indicate that the opioid receptor antagonists, naloxone and naltrexone, synergistically potentiate the suppressing effect of rimonabant on alcohol intake and alcohols motivational properties in rats. Conversely, the two clinical studies conducted to date (one in alcoholdependent individuals and one in nontreatment-seeking heavy alcohol drinkers) yielded less conclusive results. Unfortunately, the recent discontinuation - due to the occurrence of some psychiatric adverse effects - of all trials with cannabinoid CB1 receptor antagonists apparently hinders further investigations on the potential of rimonabant in the treatment of alcohol dependence.
Keywords: Cannabinoid CB1 receptor antagonists, rimonabant, alcohol, animal models of alcoholism, alcohol relapse
CNS & Neurological Disorders - Drug Targets
Title: Blockade of the Cannabinoid CB1 Receptor and Alcohol Dependence: Preclinical Evidence and Preliminary Clinical Data
Volume: 9 Issue: 1
Author(s): Paola Maccioni, Giancarlo Colombo and Mauro A.M. Carai
Affiliation:
Keywords: Cannabinoid CB1 receptor antagonists, rimonabant, alcohol, animal models of alcoholism, alcohol relapse
Abstract: The present paper summarizes the results of a number of pharmacological studies implicating the cannabinoid CB1 receptor in the neural circuitry regulating different alcohol-related behaviors in rodents. Specifically, cannabinoid CB1 receptor antagonists - including the prototype, rimonabant - have been reported to suppress: (a) acquisition and maintenance of alcohol drinking behavior under the 2-bottle “alcohol vs water” choice regimen; (b) the increase in alcohol intake occurring after a period of alcohol abstinence (an experimental model of alcohol relapse); (c) alcohols reinforcing and motivational properties measured in rats trained to perform a specific task (e.g., lever-pressing) to access alcohol; (d) reinstatement of extinguished alcohol-seeking behavior triggered in rats by a nicotine challenge or presentation of cues previously associated to alcohol availability (another model of alcohol relapse). Additional data indicate that the opioid receptor antagonists, naloxone and naltrexone, synergistically potentiate the suppressing effect of rimonabant on alcohol intake and alcohols motivational properties in rats. Conversely, the two clinical studies conducted to date (one in alcoholdependent individuals and one in nontreatment-seeking heavy alcohol drinkers) yielded less conclusive results. Unfortunately, the recent discontinuation - due to the occurrence of some psychiatric adverse effects - of all trials with cannabinoid CB1 receptor antagonists apparently hinders further investigations on the potential of rimonabant in the treatment of alcohol dependence.
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Cite this article as:
Maccioni Paola, Colombo Giancarlo and Carai A.M. Mauro, Blockade of the Cannabinoid CB1 Receptor and Alcohol Dependence: Preclinical Evidence and Preliminary Clinical Data, CNS & Neurological Disorders - Drug Targets 2010; 9 (1) . https://dx.doi.org/10.2174/187152710790966623
DOI https://dx.doi.org/10.2174/187152710790966623 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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