Zinc-mediated cell death in the hippocampus following experimental traumatic brain injury



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Traumatic brain injury (TBI) is a leading cause of morbidity and mortality of Americans both in the 15-25 age range and in the elderly population. Hippocampal neuronal damage is a key feature of experimental fluid percussion traumatic brain injury in rodents. However, the mechanisms contributing to the susceptibility to neuronal injury in this region are largely unknown. Since free ionic zinc (Zn2+) was shown to be toxic to neurons in vitro, I sought to examine the effects of Zn2+ on neuronal injury following TBI. To study this problem, I characterized a model of Zn2+-induced injury in an attempt to isolate zinc’s effect on cell death, in vivo. I also adapted a fluorimetric method to measure the amount of extracellular Zn2+ present following TBI, using microdialysis techniques. To date, the measurement of free ionic Zn2+ release in vivo after trauma has not been shown. I demonstrate that the amount of Zn2+ found in the extracellular fluid of TBI rats was below the range that causes neuronal injury and was not different than the amount of Zn2+ found in sham operated rats. Results of my experiments do not support the idea that presynaptic release of Zn2+ causes injury to surrounding neurons.



zinc, traumatic brain injury, neurotoxicity, fluid percussion injury