Previous studies have shown that pro-inflammatory cytokines were involved in the genesis and persistence of neuropathic pain. Nuclear factor kappa B (NF-kappa B) plays a crucial role in regulating pro-inflammatory cytokine gene expression. In this study, we examined the hypothesis that NF-kappa B would regulate the expression of spinal tumor necrosis factor alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS) following chronic constriction nerve injury (CCI) in rats. CCI induced a significant upregulation of NF-kappa B in the ipsilateral spinal cord on postoperative Day 7 as revealed by Western blot, immunohistochemistry and real time polymerase chain reaction (real time-PCR). Moreover, TNF-alpha mRNA expression was markedly upregulated by CCI, whereas only a low level of iNOS mRNA was detected in the ipsilateral spinal cord. The immunohistochemical data indicated a pattern of colocalization between NF-kappa B and TNF-alpha within spinal cord dorsal horn. These results show that NF-kappa B activation is correlated with TNF-alpha expression, but not iNOS expression, in the spinal cord after peripheral nerve injury.