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Although early detection and treatment are important, our understanding of pain\u2010related molecular mechanisms remains largely unclear. Here we investigate these mechanisms using an animal model for CNC injury. To confirm that CNC injury induces pain, we assessed expression of c\u2010fos, a gene that is rapidly expressed in spinal sensory afferents in response to painful peripheral stimuli, and TNF\u2010\u03b1 and IL\u20106, two proinflammatory cytokines that are crucial to development of inflammatory\u2010mediated pain. Results show c\u2010fos upregulation 1\u20132 weeks postinjury in the absence of TNF\u2010\u03b1 or IL\u20106 expression, indicating increased neural sensitivity without an inflammatory response. This is consistent with previous studies that showed no morphologic evidence of inflammation in the CNC model. Surprisingly, we also found de novo expression of Na<jats:sub>V<\/jats:sub>1.8, a sodium channel linked to the development of neuropathic pain, in endoneurial Schwann cells following injury. Until now, Na<jats:sub>V<\/jats:sub>1.8 expression was thought to be restricted to sensory neurons. CNC injury appears to be a unique model of noninflammatory neuropathic pain. Further investigation of the underlying molecular basis could yield promising targets for early diagnosis and treatment. \u00a9 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. 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