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An estimated 275,000 Americans are hospitalized following a traumatic brain injury (TBI) every year, 80,000 of whom develop a long-term disability. The factor that places one at perhaps the greatest risk of suffering a TBI is alcohol intoxication. 30-50% of TBI sufferers have a blood alcohol level above .08 mg/dl at the time of injury, the legal limit in most U.S. states. In fact, the presence of alcohol at the time of TBI more than doubles the risk of a repeat head injury in the two years following the injury. Given the large population of TBI sufferers with alcohol intoxication as a comorbidity, it is important to determine its consequences for recovery and the mechanisms by which alcohol exerts its effects on the CNS post-injury. To this end, we trained adult, male, Sprague Dawley rats on a skilled sensorimotor test, the forelimb reaching task. Following successful learning, animals were administered either a repeated binge regimen of ethanol (2g/kg) for three consecutive days or a single binge dose. One hour after the final ethanol dose, rats were given a traumatic brain injury to the sensorimotor cortex so as to produce a deficit on the skilled forelimb reaching task. Animals were then tested for seven weeks on the forelimb reaching task to assess the profile of recovery. A subset of rats were tested on the open field test 11 days after injury to measure anxiety-like behavior. We found that administration of a repeated binge regimen of ethanol delivered prior to TBI led to a slower recovery with a lower recovery plateau. In contrast, rats given a single dose of binge ethanol prior to TBI recovered faster on average than animals given a vehicle control. However, the estimated group differences in the recovery plateau were not statistically significant. Our injury did not affect behaviors in the open field test.

We next investigated whether the poorer recovery displayed by the repeated binge ethanol administered rats was correlated with a reduction in subventricular zone (SVZ) precursor cell proliferation and subsequent neuronal differentiation. We found that ethanol negatively affected SVZ precursor cell proliferation when measured 21 days after TBI. This reduction was statistically significant in both the injured and uninjured hemispheres. However, there was not a statistically significant main effect of the TBI itself, nor was there a statistically significant interaction between ethanol and the TBI on NPC density. Secondly, we found that ethanol decreased the density of immature neurons in the SVZ closest to the TBI lesion. However, we did not find that the TBI itself or the interaction between the TBI and ethanol affected immature neuronal cell density to a statistically significant degree

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