Tumor necrosis factor–Α contributes to below-level neuropathic pain after spinal cord injury
dc.contributor.author | Peng, Xiangmin | en_US |
dc.contributor.author | Zhou, Zhi-gang | en_US |
dc.contributor.author | Glorioso, Joseph C. | en_US |
dc.contributor.author | Fink, David J. | en_US |
dc.contributor.author | Mata, Marina | en_US |
dc.date.accessioned | 2007-05-02T14:16:44Z | |
dc.date.available | 2007-05-02T14:16:44Z | |
dc.date.issued | 2006-05 | en_US |
dc.identifier.citation | Peng, Xiang-min; Zhou, Zhi-gang; Glorioso, Joseph C.; Fink, David J.; Mata, Marina (2006). "Tumor necrosis factor–Α contributes to below-level neuropathic pain after spinal cord injury." Annals of Neurology 59(5): 843-851. <http://hdl.handle.net/2027.42/50655> | en_US |
dc.identifier.issn | 0364-5134 | en_US |
dc.identifier.issn | 1531-8249 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/50655 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16634039&dopt=citation | en_US |
dc.description.abstract | Objective Our objective was to elucidate the mechanisms responsible for below-level pain after partial spinal cord injury (SCI). Methods 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–Α (TNF-Α) to evaluate the role of TNF-Α in the pathogenesis of below-level pain. Results We found activation of microglia and increased expression of TNF-Α 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-Α had an apparent molecular weight of 27kDa, consistent with the full-length transmembrane form of the protein (mTNF-Α). 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-Α in the dorsal horn. Interpretation These results suggest that expression of mTNF-Α after injury is related to development of pain, and that reverse signaling through mTNF-Α by sTNFR at that level reduces cellular markers of inflammatory response and pain-related behavior. Ann Neurol 2006;59:843–851 | en_US |
dc.format.extent | 360778 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology, and Psychiatry | en_US |
dc.title | Tumor necrosis factor–Α contributes to below-level neuropathic pain after spinal cord injury | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Psychiatry | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MI | en_US |
dc.contributor.affiliationum | Department of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MI | en_US |
dc.contributor.affiliationum | Department of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MI ; Department of Neurology, University of Michigan Health System, 1500 E. Medical Center Drive, Room 1914 TC, Ann Arbor, MI 48109-0316 | en_US |
dc.contributor.affiliationum | Department of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MI | en_US |
dc.contributor.affiliationother | Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, PA | en_US |
dc.identifier.pmid | 16634039 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/50655/1/20855_ftp.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1002/ana.20855 | en_US |
dc.identifier.source | Annals of Neurology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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