• Qing Yang, Zizhen Wu, Julia K Hadden, Max A Odem, Yan Zuo, Robyn J Crook, Jeffrey A Frost, and Edgar T Walters.
• Department of Integrative Biology and Pharmacology, University of Texas Medical School at Houston, Texas, 77030 Edgar.T.Walters@uth.tmc.edu Qing.Yang@uth.tmc.edu.
• J. Neurosci. 2014 Aug 6; 34 (32): 10765-9.

AbstractChronic pain caused by insults to the CNS (central neuropathic pain) is widely assumed to be maintained exclusively by central mechanisms. However, chronic hyperexcitablility occurs in primary nociceptors after spinal cord injury (SCI), suggesting that SCI pain also depends upon continuing activity of peripheral sensory neurons. The present study in rats (Rattus norvegicus) found persistent upregulation after SCI of protein, but not mRNA, for a voltage-gated Na(+) channel, Nav1.8, that is expressed almost exclusively in primary afferent neurons. Selectively knocking down Nav1.8 after SCI suppressed spontaneous activity in dissociated dorsal root ganglion neurons, reversed hypersensitivity of hindlimb withdrawal reflexes, and reduced ongoing pain assessed by a conditioned place preference test. These results show that activity in primary afferent neurons contributes to ongoing SCI pain.Copyright © 2014 the authors 0270-6474/14/3410765-05$15.00/0.

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