Citation

Crabbe JC, Harris RA, Koob GF. Ann. N. Y. Acad. Sci. 2011; 1216(1): 24-40.

Affiliation

Portland Alcohol Research Center, Department of Behavioral Neuroscience, Oregon Health & Science University and VA Medical Center, Portland, Oregon. Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, Texas. Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, California.

Copyright

(Copyright © 2011, John Wiley and Sons)

DOI

10.1111/j.1749-6632.2010.05895.x

PMID

21272009

PMCID

PMC3076900

Abstract

Binge drinking is prevalent and has serious biomedical consequences. In children, adolescents, and young adults, it is a prominent risk factor for later development of alcohol-use disorders. Many preclinical models have been employed to study the genetic risks for and biomedical consequences of alcohol drinking. However, these models historically did not result in blood-alcohol concentrations (BACs) exceeding 80 mg%; this relatively modest level is the threshold that currently defines a binge session, according to the NIAAA and CDC. Nevertheless, in alcohol-dependent rodents, binge drinking has been well documented. Key neurobiological substrates localized to brain reward and stress systems have been identified. Studies of newer models of binge drinking without dependence are reviewed here. In these models, rodents, non-human primates, and flies will drink enough to reach high BACs. They often display observable signs of intoxication. The neurobiological consequences of these episodes of binge drinking without dependence are reviewed, and preliminary evidence for roles for GABA, glutamate, opioid peptides, and corticotropin releasing factor are discussed, as is the need for more work to identify the antecedents and consequences of binge drinking in both animal models and humans.

Language: en