Abstract
BACKGROUND: The goals of this commentary are to discuss the important contributions of the work by Kaur and colleagues titled "Corticotropin-releasing factor acting on corticotropin-releasing factor receptor type 1 is critical for binge alcohol drinking in mice," published in this issue of Alcoholism: Clinical and Experimental Research, and to highlight the importance of preclinical research aimed at identifying the neurobiology of binge ethanol drinking. METHODS AND RESULTS: The work by Kaur and colleagues provides an important extension of previous pharmacological evidence implicating the corticotropin-releasing factor (CRF) type-1 receptor (CRF1R) in binge-like ethanol drinking by verifying the role of the CRF1R using genetic tools, and by establishing that CRF, but not urocortin 1 (Ucn1), is the primary neuropeptide associated with the CRF system that modulates binge-like ethanol drinking in C57BL/6J mice. CONCLUSIONS: It is suggested that the evidence for a critical role of the CRF1R in excessive ethanol intake observed in both models of binge-like ethanol drinking and dependence-like ethanol intake indicates that overlapping mechanisms may be involved, and that studies that employ models of binge-like ethanol drinking may provide insight into the neurobiological mechanisms that underlie the transition to ethanol dependence.