Commentary: studies on binge-like ethanol drinking may help to identify the neurobiological mechanisms underlying the transition to dependence.
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.