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Article

The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats

1
Department of Acupuncture, Moxibustion and Acupoint, College of Korean Medicine, Daegu Haany University, Daegu 42158, Korea
2
Research Center for Herbal Convergence on Liver Disease, Daegu Haany University, Daegu 42158, Korea
3
Department of Biology, Valdosta State University, Valdosta, GA 31698, USA
4
Department of Physiology, College of Korean Medicine, Daegu Haany University, Daegu 42158, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Andreas von Knethen
Int. J. Mol. Sci. 2021, 22(5), 2672; https://doi.org/10.3390/ijms22052672
Received: 2 February 2021 / Revised: 28 February 2021 / Accepted: 1 March 2021 / Published: 6 March 2021
(This article belongs to the Special Issue Neuro-Plastic Mechanisms of Pain and Addiction)
Background: In the present study, we examined superoxide-mediated excitatory nociceptive transmission on at-level neuropathic pain following spinal thoracic 10 contusion injury (SCI) in male Sprague Dawley rats. Methods: Mechanical sensitivity at body trunk, neuronal firing activity, and expression of superoxide marker/ionotropic glutamate receptors (iGluRs)/CamKII were measured in the T7/8 dorsal horn, respectively. Results: Topical treatment of superoxide donor t-BOOH (0.4 mg/kg) increased neuronal firing rates and pCamKII expression in the naïve group, whereas superoxide scavenger Tempol (1 mg/kg) and non-specific ROS scavenger PBN (3 mg/kg) decreased firing rates in the SCI group (* p < 0.05). SCI showed increases of iGluRs-mediated neuronal firing rates and pCamKII expression (* p < 0.05); however, t-BOOH treatment did not show significant changes in the naïve group. The mechanical sensitivity at the body trunk in the SCI group (6.2 ± 0.5) was attenuated by CamKII inhibitor KN-93 (50 μg, 3.9 ± 0.4) or Tempol (1 mg, 4 ± 0.4) treatment (* p < 0.05). In addition, the level of superoxide marker Dhet showed significant increase in SCI rats compared to the sham group (11.7 ± 1.7 vs. 6.6 ± 1.5, * p < 0.05). Conclusions: Superoxide and the pCamKII pathway contribute to chronic at-level neuropathic pain without involvement of iGluRs following SCI. View Full-Text
Keywords: at-level; CamKII; ionotropic glutamate receptors; neuropathic pain; reactive oxygen species; spinal cord injury at-level; CamKII; ionotropic glutamate receptors; neuropathic pain; reactive oxygen species; spinal cord injury
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MDPI and ACS Style

Lee, B.H.; Kang, J.; Kim, H.Y.; Gwak, Y.S. The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats. Int. J. Mol. Sci. 2021, 22, 2672. https://doi.org/10.3390/ijms22052672

AMA Style

Lee BH, Kang J, Kim HY, Gwak YS. The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats. International Journal of Molecular Sciences. 2021; 22(5):2672. https://doi.org/10.3390/ijms22052672

Chicago/Turabian Style

Lee, Bong H., Jonghoon Kang, Hee Y. Kim, and Young S. Gwak. 2021. "The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats" International Journal of Molecular Sciences 22, no. 5: 2672. https://doi.org/10.3390/ijms22052672

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