Mitochondrial Mechanisms of Neuronal Injury
Annual rept. 1 Sep 2000-31 Aug 2001
PITTSBURGH UNIV PA
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This project is investigating the contribution of mitochondria to neuronal injury. Our previous studies have shown that glutamate mediated injury to neurons requires mitochondrial calcium accumulation. However, we know little about the magnitude of the mitochondrial calcium load that causes injury, or the mechanisms that link calcium to neuronal death. We have now characterized the properties of calcium transport, the mechanisms of mitochondrial oxidant generation, and a novel interaction between these two parameters that may be of particular relevance to Parkinsons disease. We have also identified a new property of mitochondria in the form of spontaneous mitochondrial depolarizations, and have found that this property is expressed in many different cell types. We are also investigating the properties of cytochrome c release in relation to apoptosis, which may be an important regulator of mitochondrial function. Finally, we have begun to establish a cell culture model of Parkinsons disease so that we can apply some of our studies to specific, vulnerable cell populations. These studies are providing important new information related to the control of neuronal injury by mitochondrial function.
- Medicine and Medical Research