| Varenicline, an alpha4beta2 nicotinic acetylcholine receptor partial agonist, selectively decreases ethanol consumption and seeking |
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Pia Steensland, Jeffrey A. Simms, Joan Holgate, Jemma K. Richards and Selena E. Bartlett Paper Published in PNAS July 2007 Abstract Alcohol dependence is a disease that impacts millions of individuals worldwide. There has been some progress with pharmacotherapy for alcohol-dependent individuals however there remains a critical need for the development of novel and additional therapeutic approaches. Alcohol and nicotine are commonly abused together and there is evidence that neuronal nicotinic acetylcholine receptors (nAChRs) play a role in both alcohol and nicotine dependence. Varenicline, a partial agonist at the alpha4beta2 nAChRs, reduces nicotine intake and was recently approved as a smoking cessation aid. We have investigated the role of varenicline in the modulation of ethanol consumption and seeking using three different animal models of drinking. We show that acute administration of varenicline, in doses reported to reduce nicotine reward, selectively reduced ethanol but not sucrose seeking using an operant self-administration drinking paradigm and also decreased voluntary ethanol but not water consumption in animals chronically exposed to ethanol for two months prior to varenicline treatment. Furthermore chronic varenicline administration decreased ethanol consumption and this did not result in a rebound increase in ethanol intake when the varenicline was no longer administered. The data suggest that the alpha4beta2 nAChRs may play a role in ethanol seeking behaviors in animals chronically exposed to ethanol. The selectivity of varenicline in decreasing ethanol consumption combined with its reported safety profile and mild side effects in humans suggests varenicline may prove to be a novel treatment for alcohol dependence.Watch Selena Bartlett's interviews on: CTV News, NBC Today, NineMSN View news releases at: WebMD, Voice of America, The Sacramento Bee, ABC, SF Chronicle, UCSF News Office |



