Title | Adaptations underlying the development of excessive alcohol intake in selectively bred mice. |
Publication Type | Journal Article |
Year of Publication | 2014 |
Authors | Kippin TE |
Journal | Alcohol Clin Exp Res |
Volume | 38 |
Issue | 1 |
Pagination | 36-9 |
Date Published | 2014 Jan |
ISSN | 1530-0277 |
Keywords | Adaptation, Physiological, Alcohol Drinking, Alcoholism, Animals, Crosses, Genetic, Disease Models, Animal, Disease Progression, Humans, Mice |
Abstract | BACKGROUND: This commentary discusses the important contributions of the article in this issue by Matson and colleagues entitled "Selectively bred crossed high-alcohol-preferring mice drink to intoxication and develop functional tolerance, but not locomotor sensitization during free-choice ethanol access" as well as providing comparison to studies on other drugs of abuse. METHODS: The findings of the target article are evaluated and compared to the larger literature of intake escalation and vulnerability to addiction observed with other drugs of abuse. RESULTS: In their study, Matson and colleagues report that mice derived by crossing different lines selectively bred for high alcohol intake exhibit initial alcohol intakes associated with motor impairment followed by marked escalation of consumption and tolerance to the effects of alcohol on motor coordination. In contrast, no evidence of pharmacokinetic tolerance or sensitization of alcohol-induced locomotion was observed. These results demonstrate that the cHAP mice constitute an appropriate model for the study of excessive drinking, which is produced by escalated alcohol intake and functional changes, leading to excessive intoxication. CONCLUSIONS: Future work should assess adaptations in motivational processes and subjective effects of alcohol as well as the potential genetic and epigenetic bases of escalated alcohol intake. |
DOI | 10.1111/acer.12327 |
Alternate Journal | Alcohol. Clin. Exp. Res. |
PubMed ID | 24354427 |
PubMed Central ID | PMC3951716 |
Grant List | DA027525 / DA / NIDA NIH HHS / United States R01 DA027525 / DA / NIDA NIH HHS / United States R21 DA027115 / DA / NIDA NIH HHS / United States |