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Tumor necrosis factor–Α contributes to below-level neuropathic pain after spinal cord injury

dc.contributor.authorPeng, Xiangminen_US
dc.contributor.authorZhou, Zhi-gangen_US
dc.contributor.authorGlorioso, Joseph C.en_US
dc.contributor.authorFink, David J.en_US
dc.contributor.authorMata, Marinaen_US
dc.date.accessioned2007-05-02T14:16:44Z
dc.date.available2007-05-02T14:16:44Z
dc.date.issued2006-05en_US
dc.identifier.citationPeng, 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.issn0364-5134en_US
dc.identifier.issn1531-8249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50655
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16634039&dopt=citationen_US
dc.description.abstractObjective 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;59:843–851en_US
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dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology, and Psychiatryen_US
dc.titleTumor necrosis factor–Α contributes to below-level neuropathic pain after spinal cord injuryen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment 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 48109-0316en_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan and VA Ann Arbor Healthcare System, Ann Arbor, MIen_US
dc.contributor.affiliationotherDepartment of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, PAen_US
dc.identifier.pmid16634039en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50655/1/20855_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/ana.20855en_US
dc.identifier.sourceAnnals of Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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