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Description:
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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 . |