| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1070861 | Drug and Alcohol Dependence | 2010 | 5 Pages |
BackgroundThe high rate of comorbidity of tobacco smoking with alcohol drinking suggests common neural substrates mediate the two addictive disorders. The beta2*-containing nicotinic acetylcholine receptor (β2*-nAChR) has recently emerged as a prime candidate because some alpha and beta subunit genes have been linked to alcohol consumption and alcohol use behaviors. We hypothesized that β2*-nAChR availability would be altered by alcohol in heavy drinking nonsmokers.MethodsEleven heavy drinking (mean age 39.6 ± 12.1 years) and 11 age and sex-matched control (mean age 40.8 ± 14.1 years) nonsmokers were imaged using [123I]5-IA-85380 ([123I]5-IA) single photon emission computed tomography (SPECT). Heavy alcohol drinkers drank varied amounts of alcohol (70–428/month) to facilitate exploratory linear analyses of the possible effects of alcohol.ResultsHeavy drinkers consumed on average 9.1 ± 7.3 drinks/occasion; whereas controls drank 1.2 ± 0.9 drinks/occasion. Heavy drinkers were imaged 2.0 ± 1.6 days after last alcoholic beverage. Overall, there were no significant differences in β2*-nAChR availability between the heavy drinking and control nonsmokers. Exploratory analyses of other factors that may be uniquely regulated by alcohol suggested no effects of age, number of alcohol drinks, years drinking, severity of drinking, craving or withdrawal.ConclusionsThese preliminary analyses do not suggest a decrease in receptor availability in heavy drinking nonsmokers as compared to control nonsmokers. However, a larger study is warranted to explore effects of heavy alcohol drinking on other variables, such as sex, smoking, and genetic make up.
