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- W57484554 endingPage "146" @default.
- W57484554 startingPage "119" @default.
- W57484554 abstract "Mitochondria have a variety of essential functions within neurons including oxygen consumption, ATP generation, calcium buffering, and reactive oxygen species (ROS) generation. Despite extensive research into the contribution of mitochondrial function in other neurological disorders such as Parkinson's disease, the role of mitochondrial function in sensory processing and pain has been relatively unexplored until recent years. As this area of pain research is in its infancy, this review will be a descriptive summary—rather than a critical review—of data that suggests mitochondrial function/dysfunction as a causal or contributory mechanism of normal sensory processing and chronic pain. Evidence for mitochondrial dysfunction from both chronic pain patients and animal models of chronic pain will be described. Such evidence involves different aspects of mitochondria and their function including mitochondrial ultrastructure, distribution, oxygen consumption, oxidative phosphorylation, calcium buffering, ROS, and ATP levels. Most recently, substantial amounts of data have demonstrated mitochondrial involvement in painful peripheral neuropathies evoked by chemotherapy, diabetes, and HIV and these topics will be particularly highlighted in this review." @default.
- W57484554 created "2016-06-24" @default.
- W57484554 creator A5087281051 @default.
- W57484554 date "2015-01-01" @default.
- W57484554 modified "2023-10-10" @default.
- W57484554 title "The Contribution of Mitochondria to Sensory Processing and Pain" @default.
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