Neurotoxicity From Chronic Exposure to Depleted Uranium

This project is designed to test the hypothesis that chronic exposure to depleted uranium (DU) impairs neuronal processes underlying cognitive function via alterations induced at hippocampal glutamatergic synapses. Evidence has been uncovered that suggests a direct effect of uranium to diminish stim...

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Bibliographic Details
Main Author: Lasley, Stephen M
Format: Report
Language:English
Subjects:
Anatomy and Physiology
DEPLETED URANIUM
EXPOSURE(GENERAL)
GLUTAMIC ACID
GROWTH(GENERAL)
HIPPOCAMPUS
IN VIVO ANALYSIS
NERVE CELLS
NEUROTOXINS
RECEPTOR SITES(PHYSIOLOGY)
Toxicology
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Summary:This project is designed to test the hypothesis that chronic exposure to depleted uranium (DU) impairs neuronal processes underlying cognitive function via alterations induced at hippocampal glutamatergic synapses. Evidence has been uncovered that suggests a direct effect of uranium to diminish stimulated hippocampal glutamate release which may account for the reported decrease in neuronal excitability (3). However other findings indicate that long-term DU exposure may also inhibit glial glutamate and GABA uptake and up-regulate NMDA receptors possibly predisposing the individual to excitotoxicity and neurodegenerative disease. The establishment of the DU chronic exposure protocol as a shrapnel wound model based on blood and brain levels of the metal and altered rates of growth is also notable. These measures provide benchmark values for future studies and for correlation of results from this project to those obtained in other laboratories. Given the similarity of the effects of uranium on transmitter release to those of other multivalent metals (e.g. methylmercury lead) and the fact that exposure in military scenarios is continuing it is clear that additional studies are warranted on uranium's actions, particularly those related to developmental neurotoxicity. The original document contains color images.