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Neurotoxicity From Chronic Exposure to Depleted Utanium

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Annual rept. 1 Apr 2004-31 Mar 2005

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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 As prescribed by the Statement of Work, efforts in year 3 concerned achievement of substantial progress on Technical Objective 2 defining 0 integrity of hippocampal glutamate release and initiating Technical Objective 3 identifying changes in glutamate receptor subtypes. Acute exposure to U in vitro diminished K-stimulated glutamate and GABA release in a concentration dependent fashion in hippocampal synaptosomes, but the inhibitory effect on evoked glutamate release was substantially more potent ICsub 50 2.77 muM than that on GABA release,lease ICSUB 50 3.20 mM. Depolarization of superfused hippocampal synaptosomes with high K in Caexp 2-free buffer evoked modest increases in glutamate and GABA release, but acute uranium exposure in vitro across a range of concentrations did not exhibit Caexp 2-mimetic properties on transmitter release. Studies are currently underway examining the effects of chronic exposure on transmitter release in vivo and investigating the actions of acute U on NMDA receptor function. Given the similarity of effects of U on transmitter release to those of other multivalent metals and the fact that exposure in military scenarios is continuing, additional studies are warranted on uranium actions in several experimental settings.

Subject Categories:

  • Anatomy and Physiology
  • Toxicology
  • Radioactivity, Radioactive Wastes and Fission Products

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