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We here investigated whether TNFR1 regulates IL\u20106 expression through NF\u2010\u03baB or p38 MAPK activations in the spinal cord and DRG in rats with chronic constriction injury (CCI) of the sciatic nerve. Intrathecal treatment with a TNFR1 antisense oligonucleotide (ASO) significantly inhibited CCI\u2010elevated IKKs phosphorylation, IkB\u2010\u03b1 degradation, the nuclear translocation, phosphorylation, and DNA\u2010binding activity of NF\u2010\u03baB, p38 MAPK activation, and IL\u20106 mRNA and protein expression in the spinal cord and DRG. Interestingly, CCI remarkably elevated IKK\u03b1 and p65 phosphorylations in the spinal cord rather than in the DRG. In addition, NF\u2010\u03baB decoy, but not p38 MAPK inhibitor, SB203580 reduced CCI\u2010elevated IL\u20106 expression in the spinal cord and DRG. Therefore, these data suggest that TNFR1 induces IL\u20106 upregulation and neuropathic pain through NF\u2010\u03baB, but not p38 MAPK activation in the spinal cord and DRG and that the NF\u2010\u03baB\/IL\u20106 pathways in the DRG may be less dependent on TNFR1 than the spinal cord pathway.<\/jats:p>","DOI":"10.1016\/j.ejpain.2008.09.009","type":"journal-article","created":{"date-parts":[[2008,10,20]],"date-time":"2008-10-20T08:26:01Z","timestamp":1224491161000},"page":"794-806","source":"Crossref","is-referenced-by-count":62,"title":["Tumor necrosis factor receptor 1 induces interleukin\u20106 upregulation through NF\u2010kappaB in a rat neuropathic pain 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