Traumatic Brain Injury Lab Report

Traumatic brain injury (TBI) is a multi-faceted injury and is considered the leading cause of ailment in soldiers and pedestrians. During injury, a surge in ROS facilitates a vicious cycle that accelerates mitochondrial damage, excitotoxicity, lipid peroxidation, and inflammation. Further, mitochondrial targeting strategies in TBI have been increasingly studied as their maintenance will potentially preserve brain function. Melatonin is one such mitochondrial targeted strategy. Melatonin is synthesized naturally with in the body. Melatonin acts as the bodies sleep and wake system, that allows it to redirect electrons to the mitochondrial ETC, thereby enhancing ATP production and promoting cell survival. In bypassing complex I-III activity, Melatonin reduces ROS production from the mitochondrial ETC, which has the potential to minimize ischemic and reperfusion injury. TBI was induced over the S1 region of the cortex in male Sprague

ATP content and mitochondrial respiration will be measured ex vivo in rats selected from Experiment 2A at each time point (0-3 hours, 2 and 7 days) to determine the effects of melatonin on mitochondrial energetics and ROS production. Data generated will allow a comparison to be done of ex vivo ATP content and mitochondrial respiration rates in lesion versus non-lesion with in vivo measures of ATP status obtained using MRI in the same rat. Comparison will be made between saline and melatonin treated rats.

Experiment 1C: To determine the impact of mono therapy (Melatonin) following TBI on apoptotic markers. Fluro Jade B and Nissl staining will be measured ex vivo in rats selected from Experiment 1A at each time point (0-3 hours, 2 and 7 days) to determine the effects of melatonin on apoptosis. Comparison will be made between saline and melatonin treated rats in terms of induction of apoptosis and morphological