A novel and robust conditioning lesion induced by ethidium bromide. Academic Article uri icon

Overview

abstract

  • Molecular and cellular mechanisms underlying the peripheral conditioning lesion remain unsolved. We show here that injection of a chemical demyelinating agent, ethidium bromide, into the sciatic nerve induces a similar set of regeneration-associated genes and promotes a 2.7-fold greater extent of sensory axon regeneration in the spinal cord than sciatic nerve crush. We found that more severe peripheral demyelination correlates with more severe functional and electrophysiological deficits, but more robust central regeneration. Ethidium bromide injection does not activate macrophages at the demyelinated sciatic nerve site, as observed after nerve crush, but briefly activates macrophages in the dorsal root ganglion. This study provides a new method for investigating the underlying mechanisms of the conditioning response and suggests that loss of the peripheral myelin may be a major signal to change the intrinsic growth state of adult sensory neurons and promote regeneration.

publication date

  • December 23, 2014

Research

keywords

  • Ethidium
  • Nerve Crush
  • Nerve Regeneration
  • Sciatic Nerve

Identity

PubMed Central ID

  • PMC4346483

Scopus Document Identifier

  • 84925258705

Digital Object Identifier (DOI)

  • 10.1016/j.expneurol.2014.12.004

PubMed ID

  • 25541322

Additional Document Info

volume

  • 265