Traumatic brain injury is a major cause of death and disability, and many people are under the influence of alcohol at the time of injury, following a pattern of binge alcohol use. Neuroinflammation is a consequence of traumatic brain injury, and alcohol has been shown to have a modulatory effect on the brain inflammatory response through interactions with microglial cells. Additionally, exposure to binge alcohol decreases dendritic complexity of pyramidal neurons in the neocortex, leading to poor performance on behavioral tasks. Therefore, we hypothesize that: Binge ethanol exposure prior to traumatic brain injury will worsen functional outcome and decrease neuronal plasticity due to an increase in the neuroinflammatory response.
Aim #1 will determine functional recovery and neuronal plasticity in adult male rats given a binge ethanol regimen followed by traumatic brain injury while acutely intoxicated. We will use sensitive tests of sensorimotor recovery and golgi-cox staining to determine neuronal dendritic plasticity.
Aim #2 will determine the neuroinflammatory response in adult rats given a binge ethanol regimen followed by traumatic brain injury while acutely intoxicated. We will determine inflammatory cytokine levels and characterize the microglial cell response in pertinent brain regions.
Traumatic brain injury is a devastating condition which can result in poor recovery and severe neurological deficits. This type of injury often occurs while under the influence of alcohol, although little is known in regards to the resultant neuroinflammatory environment and this effect on neuronal plasticity and functional recovery. Information gained from the present proposal may lead to novel therapeutic strategies to improve outcome after traumatic brain injury and binge alcohol use.
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