Effects of Mild Traumatic Brain Injury on Ethanol Consumption and the Combined Effects on Neuroinflammation, Cognition, and Behavior in Mice

The relationship between alcohol consumption and traumatic brain injury (TBI) often focuses on alcohol consumption increasing the likelihood of incurring a TBI, rather than alcohol use outcomes after TBI. This focus is in part due to the large numbers of TBI patients visiting emergency rooms notable levels of alcohol in their blood. Additionally, increases in alcohol use disorders following TBI can be predicted by previous history of alcohol use. However, studies have also shown patients without a history of an alcohol use disorder can experience increases in problem drinking after single or multiple TBIs. Due to the diffuse impact of alcohol consumption and mild TBI on the brain, it is likely that an interaction exists between TBI outcomes and problematic alcohol use after TBI. To examine the impact of mild repetitive TBI (rmTBI) on voluntary alcohol consumption, male mice were subjected to four mild TBI or sham procedures over a two week period, then offered ethanol (20% v/v) for 2, 4, 6 or 8 weeks using the two-bottle choice, drinking in the dark paradigm. Following the drinking period, mice were sacrificed and brains were extracted to examine expression of the pro-inflammatory cytokine TNF-α, a possible shared mechanism of neuronal damage. An additional cohort of mice was subjected to the same rmTBI and voluntary ethanol paradigm and tested for cognitive and behavioral deficits following the set drinking period. Results indicate there is a temporary decrease in ethanol consumption following rmTBIs compared to Sham mice in this model. Results also suggest an attenuated expression of TNF-α in rmTBI, ethanol drinking groups compared to ethanol exposed mice after the Sham procedure. The outcomes of the cognitive and behavioral tasks suggest that ethanol consumption after rmTBI can cause transient cognitive dysfunction and increased novelty preference