0294 Voluntary Alcohol Consumption and Sleep Deprivation in Rats

Abstract

Abstract Introduction Alcohol is one of the most common psychoactive drugs that has depressant effects on the central nervous system. The vast majority of research on alcohol and sleep indicates chronic alcohol consumption has a detrimental impact on sleep architecture and homeostasis. However, less research has explored the effects of sleep deprivation on alcohol consumption; that is, the relationship in the opposite direction. Previous animal studies have explored a potential bi-directional relationship between sleep and alcohol with promising results. However, there was concern that the potential relationship may be a result of stress as a by-product of the sleep deprivation method. The present study examines the effect of sleep deprivation on voluntary alcohol consumption using two sleep deprivation methods in the rat, forced exercise wheels and the automated sleep deprivation system. Methods Twelve male Sprague-Dawley rats had ad libitum access to a 7% alcohol solution and water. Alcohol and water consumption was measured daily at 0900. Baseline consumption levels were recorded in the home cage prior to introduction to the sleep deprivation equipment. Following baseline, rats were placed in the stationary equipment for the first sleep deprivation environment control. Rats were then subjected to 6hr/day of sleep deprivation for five consecutive days in either the forced exercise wheel (n=6) or the automated sleep deprivation system (n=6). After sleep deprivation, rats were placed back in the stationary equipment as a second control measure. In total, there were four conditions, home cage baseline, first sleep deprivation environment control, sleep deprivation, second environment control. Results Data indicates that rats consumed significantly more alcohol in the sleep deprivation condition and the second sleep deprivation control. There was no difference between the two sleep deprivation methods. The mean alcohol consumption (g/kg) significantly increased from the sleep deprivation condition to the second environment control indicating a cumulative effect. Conclusion The increase in alcohol consumption in the final condition rejects the hypothesis of a bi-directional relationship. Instead, the data suggests potential receptor downregulation due to alcohol exposure over time and a conditioned compensatory effect of the sleep deprivation environment. Research methodology issues also may have confounded results. Support (If Any)