Spinal cord injury triggers an intrinsic growth-promoting state in nociceptors

Supinder S. Bedi, Michael T. Lago, Luke I. Masha, Robyn J. Crook, Raymond J. Grill, Edgar T. Walters

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Although most investigations of the mechanisms underlying chronic pain after spinal cord injury (SCI) have examined the central nervous system (CNS), recent studies have shown that nociceptive primary afferent neurons display persistent hyperexcitability and spontaneous activity in their peripheral branches and somata in dorsal root ganglia (DRG) after SCI. This suggests that SCI-induced alterations of primary nociceptors contribute to central sensitization and chronic pain after SCI. Does SCI also promote growth of these neurons' fibers, as has been suggested in some reports? The present study tests the hypothesis that SCI induces an intrinsic growth-promoting state in DRG neurons. This was tested by dissociating DRG neurons 3 days or 1 month after spinal contusion injury at thoracic level T10 and measuring neuritic growth 1 day later. Neurons cultured 3 days after SCI exhibited longer neurites without increases in branching ("elongating growth"), compared to neurons from sham-treated or untreated (naïve) rats. Robust promotion of elongating growth was found in small and medium-sized neurons (but not large neurons) from lumbar (L3-L5) and thoracic ganglia immediately above (T9) and below (T10-T11) the contusion site, but not from cervical DRG. Elongating growth was also found in neurons immunoreactive to calcitonin gene-related peptide (CGRP), suggesting that some of the neurons exhibiting enhanced neuritic growth were nociceptors. The same measurements made on neurons dissociated 1 month after SCI revealed no evidence of elongating growth, although evidence for accelerated initiation of neurite outgrowth was found. Under certain conditions this transient growth-promoting state in nociceptors might be important for the development of chronic pain and hyperreflexia after SCI.

Original languageEnglish (US)
Pages (from-to)925-935
Number of pages11
JournalJournal of neurotrauma
Volume29
Issue number5
DOIs
StatePublished - Mar 20 2012
Externally publishedYes

Keywords

  • calcitonin gene-related peptide
  • conditioning lesion
  • pain
  • primary afferent
  • regeneration

ASJC Scopus subject areas

  • Clinical Neurology

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