Persistent pain after spinal cord injury is maintained by primary afferent activity

Qing Yang, Zizhen Wu, Julia K. Hadden, Max A. Odem, Yan Zuo, Robyn J. Crook, Jeffrey A. Frost, Edgar T. Walters

Research output: Contribution to journalArticle

52 Scopus citations

Abstract

Chronic 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.

Original languageEnglish (US)
Pages (from-to)10765-10769
Number of pages5
JournalJournal of Neuroscience
Volume34
Issue number32
DOIs
StatePublished - Aug 6 2014
Externally publishedYes

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Keywords

  • Chronic pain
  • Dorsal root ganglion
  • Nav1.8
  • Neuropathic pain
  • Nociceptor
  • Spinal contusion

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Yang, Q., Wu, Z., Hadden, J. K., Odem, M. A., Zuo, Y., Crook, R. J., Frost, J. A., & Walters, E. T. (2014). Persistent pain after spinal cord injury is maintained by primary afferent activity. Journal of Neuroscience, 34(32), 10765-10769. https://doi.org/10.1523/JNEUROSCI.5316-13.2014