Commentary: Studies on Binge-Like Ethanol Drinking May Help to Identify the Neurobiological Mechanisms Underlying the Transition to Dependence
Reprint requests: Todd E. Thiele, Department of Psychology, University of North Carolina, Davie Hall CB# 3270, Chapel Hill, NC 27599-3270; Tel.: 919-962-1519; Fax: 919-962-2537; E-mail:email@example.com
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.
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.