Abstract
Binge alcohol (ethanol) drinking is a destructive pattern of ethanol consumption that may precipitate ethanol dependence-a chronic, debilitating, and prevalent health problem. While an abundance of research has focused on the neurochemical underpinnings of ethanol dependence, relatively little is known about the mechanisms underlying the heavy consumption characteristic of binge ethanol drinking. Recently, a simple preclinical model termed "drinking in the dark" (DID) was developed to examine binge-like ethanol consumption in a rodent population. This assay capitalizes on the predisposition of C57BL/6J mice to voluntarily consume substantial quantities of a high concentration (20% v/v) ethanol solution, resulting in pharmacologically relevant blood ethanol concentrations (BECs). This review provides a comprehensive overview of recent literature utilizing this model to investigate the neuromodulatory systems that may influence binge ethanol drinking. Studies examining the glutamatergic and opioidergic systems not only provide evidence for these systems in the modulation of binge-like ethanol consumption, but also suggest this preclinical model has predictive validity and may be an appropriate tool for screening novel pharmacological compounds aimed at treating binge ethanol drinking in the human population. Additionally, this review presents evidence for the involvement of the GABAergic, dopaminergic, nicotinic, and endocannabinoid systems in modulating binge-like ethanol consumption. Finally, recent evidence shows that corticotropin-releasing factor (CRF), agouti-related protein (AgRP), neuropeptide Y (NPY), and ghrelin are also implicated as impacting this pattern of ethanol consumption.