Involvement of peripheral and spinal tumor necrosis factor α in spinal cord hyperexcitability during knee joint inflammation in rats.

摘要: Objective Tumor necrosis factor α (TNFα) is produced not only in peripheral tissues, but also the spinal cord. The purpose of this study was to address potential and TNFα induce maintain hyperexcitability, which a hallmark pain states joints during rheumatoid arthritis osteoarthritis. Methods In vivo recordings responses cord neurons nociceptive knee input under normal conditions presence experimental joint inflammation were obtained anesthetized rats. TNFα, etanercept, or antibodies TNF receptors applied either surface. Results Injection into cavity increased mechanical stimulation, injection etanercept reduced inflammation-evoked activity. These effects closely mirrored induction reduction sensitization. Responses stimulation enhanced by application anti–TNF receptor type I significantly attenuated generation characterized widespread sensitization beyond inflamed joint. Spinally did reduce established hyperexcitability acute kaolin/carrageenan model. In antigen-induced arthritis, decreased on day 1, 3. Conclusion While increases supports full pattern hyperexcitability. However, may be maintained downstream mechanisms that are independent TNFα.