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The Journal of Neuroscience, January 7, 2009, 29(1):159-168; doi:10.1523/JNEUROSCI.3792-08.2009

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Development/Plasticity/Repair
Persistent Pain Is Dependent on Spinal Mitochondrial Antioxidant Levels

Erica S. Schwartz,¹ Hee Young Kim,¹ Jigong Wang,¹ Inhyung Lee,¹ Eric Klann,² Jin Mo Chung,¹ and Kyungsoon Chung¹

¹Department of Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston, Texas 77555-1069, and ²Center for Neural Science, New York University, New York, New York 10003

Correspondence should be addressed to Dr. Kyungsoon Chung, Department of Neuroscience and Cell Biology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1069. Email: kchung{at}utmb.edu

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.

Key words: oxidative stress; persistent pain; central sensitization; SOD-2; superoxide; mitochondria

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Received Aug. 11, 2008; revised Sept. 25, 2008; accepted Nov. 12, 2008.

Correspondence should be addressed to Dr. Kyungsoon Chung, Department of Neuroscience and Cell Biology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1069. Email: kchung{at}utmb.edu

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