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 journalArticlepeer-review

93 Scopus citations


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
Issue number32
StatePublished - Aug 6 2014
Externally publishedYes


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

ASJC Scopus subject areas

  • General Neuroscience


Dive into the research topics of 'Persistent pain after spinal cord injury is maintained by primary afferent activity'. Together they form a unique fingerprint.

Cite this