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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Blotting, Western, Enzyme-Linked Immunosorbent Assay, Female, Genetic Vectors, Immunohistochemistry, Microglia, Pain, Rats, Rats, Sprague-Dawley, Receptors, Tumor Necrosis Factor, Type I, Simplexvirus, Spinal Cord Injuries, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
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Does tumor necrosis factor-alpha contribute to below-level neuropathic pain after spinal cord injury? Context: Our objective was to elucidate the mechanisms responsible for below-level pain after partial spinal cord injury (SCI). We used lateral hemisection to model central neuropathic pain and herpes simplex viral (HSV) vector-mediated transfer of the cleaved soluble receptor for tumor necrosis factor-alpha (TNF-alpha) to evaluate the role of TNF-alpha in the pathogenesis of below-level pain. We found activation of microglia and increased expression of TNF-alpha below the level of the lesion in the lumbar spinal cord after T13 lateral hemisection that correlated with emergence of mechanical allodynia in the hind limbs of rats. Lumbar TNF-alpha had an apparent molecular weight of 27 kDa, consistent with the full-length transmembrane form of the protein (mTNF-alpha). Expression of the p55 TNF soluble receptor (sTNFRs) by HSV-mediated gene transfer resulted in reduced pain behavior and a decreased number of ED1-positive cells, as well as decreased phosphorylation of the p38 MAP kinase (p-p38) and diminished expression of mTNF-alpha in the dorsal horn.
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These results suggest that expression of mTNF-alpha after injury is related to development of pain, and that reverse signaling through mTNF-alpha by sTNFR at that level reduces cellular markers of inflammatory response and pain-related behavior. Final Decision: yes