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Voluntary Alcohol Intake following Blast Exposure in a Rat Model of Mild Traumatic Brain Injury. PLoS One 2015;10(4):e0125130

Date

04/25/2015

Pubmed ID

25910266

Pubmed Central ID

PMC4409117

DOI

10.1371/journal.pone.0125130

Scopus ID

2-s2.0-84929322542 (requires institutional sign-in at Scopus site)   32 Citations

Abstract

Alcoholism is a frequent comorbidity following mild traumatic brain injury (mTBI), even in patients without a previous history of alcohol dependence. Despite this correlational relationship, the extent to which the neurological effects of mTBI contribute to the development of alcoholism is unknown. In this study, we used a rodent blast exposure model to investigate the relationship between mTBI and voluntary alcohol drinking in alcohol naïve rats. We have previously demonstrated in Sprague Dawley rats that blast exposure leads to microstructural abnormalities in the medial prefrontal cortex (mPFC) and other brain regions that progress from four to thirty days. The mPFC is a brain region implicated in alcoholism and drug addiction, although the impact of mTBI on drug reward and addiction using controlled models remains largely unexplored. Alcohol naïve Sprague Dawley rats were subjected to a blast model of mTBI (or sham conditions) and then tested in several common measures of voluntary alcohol intake. In a seven-week intermittent two-bottle choice alcohol drinking test, sham and blast exposed rats had comparable levels of alcohol intake. In a short access test session at the conclusion of the two-bottle test, blast rats fell into a bimodal distribution, and among high intake rats, blast treated animals had significantly elevated intake compared to shams. We found no effect of blast when rats were tested for an alcohol deprivation effect or compulsive drinking in a quinine adulteration test. Throughout the experiment, alcohol drinking was modest in both groups, consistent with other studies using Sprague Dawley rats. In conclusion, blast exposure had a minimal impact on overall alcohol intake in Sprague Dawley rats, although intake was increased in a subpopulation of blast animals in a short access session following intermittent access exposure.

Author List

Lim YW, Meyer NP, Shah AS, Budde MD, Stemper BD, Olsen CM

Authors

Matthew Budde PhD Associate Professor in the Neurosurgery department at Medical College of Wisconsin
Christopher M. Olsen PhD Associate Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin
Brian Stemper PhD Professor in the Biomedical Engineering department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Alcohol Drinking
Alcoholism
Animals
Brain Injuries
Choice Behavior
Disease Models, Animal
Drinking
Ethanol
Male
Prefrontal Cortex
Rats
Rats, Sprague-Dawley
Reward
Substance-Related Disorders