Partial nerve injury induces electrophysiological changes in conducting (uninjured) nociceptive and nonnociceptive DRG neurons: Possible relationships to aspects of peripheral neuropathic pain and paresthesias

Laiche Djouhri, Xin Fang, Stella Koutsikou, Sally N. Lawson*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)

60 Citations (Scopus)

Abstract

Partial nerve injury leads to peripheral neuropathic pain. This injury results in conducting/uninterrupted (also called uninjured) sensory fibres, conducting through the damaged nerve alongside axotomised/degenerating fibres. In rats seven days after L5 spinal nerve axotomy (SNA) or modified-SNA (added loose-ligation of L4 spinal nerve with neuroinflammation-inducing chromic-gut), we investigated a) neuropathic pain behaviours and b) electrophysiological changes in conducting/uninterrupted L4 dorsal root ganglion (DRG) neurons with receptive fields (called: L4-receptive-field-neurons). Compared to pretreatment, modified-SNA rats showed highly significant increases in spontaneous-foot-lifting duration, mechanical-hypersensitivity/allodynia, and heat-hypersensitivity/hyperalgesia, that were significantly greater than after SNA, especially spontaneous-foot-lifting. We recorded intracellularly in vivo from normal L4/L5 DRG neurons and ipsilateral L4-receptive-field-neurons. After SNA or modified-SNA, L4-receptive-field-neurons showed the following: a) increased percentages of C-, Ad-, and Ab-nociceptors and cutaneous Aa/b-low-threshold mechanoreceptors with ongoing/spontaneous firing; b) spontaneous firing in C-nociceptors that originated peripherally; this was at a faster rate in modified-SNA than SNA; c) decreased electrical thresholds in A-nociceptors after SNA; d) hyperpolarised membrane potentials in A-nociceptors and Aa/b-low-threshold-mechanoreceptors after SNA, but not C-nociceptors; e) decreased somatic action potential rise times in C- and A-nociceptors, not Aa/b-low-threshold-mechanoreceptors. We suggest that these changes in subtypes of conducting/uninterrupted neurons after partial nerve injury contribute to the different aspects of neuropathic pain as follows: spontaneous firing in nociceptors to ongoing/spontaneous pain; spontaneous firing in Aa/b-low-threshold-mechanoreceptors to dysesthesias/paresthesias; and lowered A-nociceptor electrical thresholds to A-nociceptor sensitization, and greater evoked pain. (C) 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Original languageEnglish
Pages (from-to)1824-1836
Number of pages13
JournalPAIN
Volume153
Issue number9
DOIs
Publication statusPublished - Sep 2012

Keywords

  • Uninjured neuron
  • Spontaneous firing
  • Dorsal root ganglion
  • Nociceptor
  • Pain behaviour
  • Nerve injury
  • Nociception
  • Neuropathic pain
  • Threshold
  • Allodynia
  • Hyperalgesia
  • Neuroinflammation
  • Spontaneous pain
  • Paresthesia
  • Action potential
  • Membrane potential
  • In vivo
  • Intracellular recording
  • A beta-nociceptors
  • A-fibre nociceptors
  • C-fibre nociceptors
  • Low-threshold mechanoreceptors
  • DORSAL-ROOT GANGLION
  • PRIMARY AFFERENT NEURONS
  • PRIMARY SENSORY NEURONS
  • ACTION-POTENTIAL SHAPE
  • GUINEA-PIG
  • SODIUM-CHANNELS
  • IN-VIVO
  • MEMBRANE-PROPERTIES
  • INFLAMMATORY PAIN
  • TACTILE ALLODYNIA

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