International Journal of Molecular Sciences | |
The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats | |
BongHyo Lee1  Jonghoon Kang2  YoungS. Gwak3  HeeYoung Kim4  | |
[1] Department of Acupuncture, Moxibustion and Acupoint, College of Korean Medicine, Daegu Haany University, Daegu 42158, Korea;Department of Biology, Valdosta State University, Valdosta, GA 31698, USA;Department of Physiology, College of Korean Medicine, Daegu Haany University, Daegu 42158, Korea;Research Center for Herbal Convergence on Liver Disease, Daegu Haany University, Daegu 42158, Korea; | |
关键词: at-level; CamKII; ionotropic glutamate receptors; neuropathic pain; reactive oxygen species; spinal cord injury; | |
DOI : 10.3390/ijms22052672 | |
来源: DOAJ |
【 摘 要 】
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 mg, 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.
【 授权许可】
Unknown