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Persistent Pain Is Dependent on Spinal Mitochondrial Antioxidant Levels

Cited 0 time in webofscience Cited 78 time in scopus
Authors
Schwartz, Erica S.; Kim, Hee Young; Wang, Jigong; Lee, Inhyung; Klann, Eric; Chung, Jin Mo; Chung, Kyungsoon
Issue Date
2009
Publisher
Society for Neuroscience
Citation
J Neurosci 29:159-168
Keywords
oxidative stresspersistent paincentral sensitizationSOD-2superoxidemitochondria
Abstract
Reactive oxygen species (ROS) scavengers have been shown to relieve persistent pain; however, the mechanism is not clearly understood.
Superoxide produced from mitochondrial oxidative phosphorylation is considered the major source of ROS in neurons during excitation
where mitochondrial superoxide levels are normally controlled by superoxide dismutase (SOD-2). The present study hypothesizes that
capsaicin-induced secondary hyperalgesia is a consequence of superoxide build-up in spinal dorsal horn neurons and SOD-2 is a major
determinant. To test this hypothesis, the spinal levels of SOD-2 activity, inactivated SOD-2 proteins, and mitochondrial superoxide were
measured and correlated to the levels of capsaicin-induced secondary hyperalgesia in mice with and without SOD-2 manipulations. The
data suggest that superoxide accumulation is a culprit in the abnormal sensory processing in the spinal cord in capsaicin-induced
secondary hyperalgesia. Our studies also support the notion that SOD-2 nitration is a critical mechanism that maintains elevated
superoxide levels in the spinal cord after capsaicin treatment. Finally, our findings suggest a therapeutic potential for the manipulation
of spinal SOD-2 activity in pain conditions.
ISSN
0270-6474
Language
English
URI
http://hdl.handle.net/10371/8613
DOI
https://doi.org/10.1523/JNEUROSCI.3792-08.2009
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College of Veterinary Medicine (수의과대학)Dept. of Veterinary Medicine (수의학과)Journal Papers (저널논문_수의학과)
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