“Wired,” Yet Intoxicated: Modeling Binge Caffeine and Alcohol Co-Consumption in the Mouse
Article first published online: 24 JUN 2014
Copyright © 2014 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 38, Issue 8, pages 2269–2278, August 2014
How to Cite
Fritz, B. M., Companion, M. and Boehm, S. L. (2014), “Wired,” Yet Intoxicated: Modeling Binge Caffeine and Alcohol Co-Consumption in the Mouse. Alcoholism: Clinical and Experimental Research, 38: 2269–2278. doi: 10.1111/acer.12472
- Issue published online: 22 AUG 2014
- Article first published online: 24 JUN 2014
- Manuscript Accepted: 16 APR 2014
- Manuscript Received: 30 JAN 2014
- NIAAA. Grant Numbers: AA016789, AA07462
The combination of highly caffeinated “energy drinks” with alcohol (ethanol [EtOH]) has become popular among young adults and intoxication via such beverages has been associated with an elevated risk for harmful behaviors. However, there are discrepancies in the human literature regarding the effect of caffeine on alcohol intoxication, perhaps due to confounding factors such as personality type, expectancy, and history of exposure. Animal models of co-exposure are resistant to such issues; however, the consequences of voluntary co-consumption have been largely ignored in the animal literature. The primary goal of this work was to characterize a mouse model of binge caffeine and EtOH co-consumption employing the limited access “Drinking-in-the-Dark” (DID) paradigm.
Caffeine was added to a 20% alcohol solution via DID. Alcohol/caffeine intake, locomotor behavior, ataxia, anxiety-like behavior, and cognitive function were evaluated as a consequence of co-consumption in adult male C57BL/6J mice.
Caffeine did not substantially alter binge alcohol intake or resultant blood EtOH concentrations (BECs), nor did it alter alcohol's anxiolytic effects on the elevated plus maze or cognitive-interfering effects in a novel object-recognition task. However, no evidence of alcohol-induced sedation was observed in co-consumption groups that instead demonstrated a highly stimulated state similar to that of caffeine alone. The addition of caffeine was also found to mitigate alcohol-induced ataxia.
Taken together, our mouse model indicates that binge co-consumption of caffeine and alcohol produces a stimulated, less ataxic and anxious, as well as cognitively altered state; a state that could be of great public health concern. These results appear to resemble the colloquially identified “wide awake drunk” state that individuals seek via consumption of such beverages. This self-administration model therefore offers the capacity for translationally valid explorations of the neurobiological consequences of binge co-consumption to assess the public health risk of this drug combination.