AbstractBinge alcohol drinking, a risky pattern of alcohol consumption, has severe consequences toward health and well‐being of an individual, his family, and society. Although, binge drinking has detrimental effects on sleep, underlying mechanisms are unknown. We used adult male C57BL/6J mice and exposed them to a single, 4‐h session of binge alcohol self‐administration, in stress‐free environment, to examine neuronal mechanisms affecting sleep. We first verified binge pattern of alcohol consumption. When allowed to self‐administer alcohol in a non‐stressful environment, mice consumed alcohol in a binge pattern. Next, effect of binge drinking on sleep–wakefulness was monitored. While sleep–wakefulness remained unchanged during drinking session, significant increase in non‐rapid eye movement (NREM) sleep was observed during 4 h of active period post‐binge, followed by increased wakefulness, reduced sleep during subsequent sleep (light) period; although the timing of sleep onset (at lights‐on) remained unaffected. Next, electrophysiological and biochemical indicators of sleep homeostasis were examined using sleep deprivation‐recovery sleep paradigm. Mice exposed to binge drinking did not show an increase in cortical theta power and basal forebrain adenosine levels during sleep deprivation; NREM sleep and NREM delta power did not increase during recovery sleep suggesting that mice exposed to binge alcohol do not develop sleep pressure. Our final experiment examined expression of genes regulating sleep homeostasis following binge drinking. While binge drinking did not affect adenosine kinase and A1 receptor, expression of equilibrative nucleoside transporter 1 (ENT1) was significantly reduced. These results suggest that binge alcohol consumption‐induced down‐regulation of ENT1 expression may disrupt sleep homeostasis and cause sleep disturbances.Open Science: This manuscript was awarded with the Open Materials Badge. For more information see: https://cos.io/our-services/open-science-badges/ image