Increased alcohol consumption in sleep-restricted rats is mediated by delta FosB induction.

The reduction of sleep hours is a public health problem in contemporary society. It is estimated that humans sleep between 1.5 and 2 h less, per night, than 100 years ago. The reduction of sleep hours is a risk factor for developing cardiovascular, metabolic, and psychiatric problems. Previous studies have shown that low sleep quality is a factor that favors relapse in addicted patients. In rodents, sleep deprivation increases the preference for methylphenidate and the self-administration of cocaine. However, it is unknown whether chronic sleep restriction induces voluntary alcohol consumption in rats and whether alcohol intake is associated with delta FosB expression in the brain reward circuit. Potentially, chronic sleep restriction could make the brain vulnerable and consequently promote addictive behavior. Therefore, the present study's objective was to evaluate alcohol consumption in a chronic sleep restriction model and determine the expression of delta FosB in brains of adult rats. For this purpose, male Wistar rats (300-350 g body weight) were divided into four experimental groups (n = 6 each group): control (without manipulation), sleep restriction (SR) for 7 days, SR and ethanol exposure (Ethanol + SR), and a group with just ethanol exposure (Ethanol). At the end of the management, rats were sacrificed, and the brains were dissected and processed for immunohistochemical detection of delta FosB. The results showed that SR stimulates alcohol consumption compared to unrestricted-sleep rats and induces a significant increase in the number of delta FosB-positive cells in brain nuclei within the motivation/brain reward circuit. These results suggest that chronic reduction of sleep hours is a risk factor for developing a preference for alcohol consumption.