lansbergen
Senior Member
- Messages
- 2,512
http://www.jneurosci.org/content/29/1/159.long
Development/Plasticity/Repair
Persistent Pain Is Dependent on Spinal Mitochondrial Antioxidant Levels
Erica S. Schwartz1, Hee Young Kim1, Jigong Wang1, Inhyung Lee1, Eric Klann2, Jin Mo Chung1, 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
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.
Development/Plasticity/Repair
Persistent Pain Is Dependent on Spinal Mitochondrial Antioxidant Levels
Erica S. Schwartz1, Hee Young Kim1, Jigong Wang1, Inhyung Lee1, Eric Klann2, Jin Mo Chung1, 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
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.