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

Djouhri, L, Fang, Xin, Koutsikou, Stella, Lawson, S N (2012) Partial nerve injury induces electrophysiological changes in conducting (uninjured) nociceptive and nonnociceptive DRG neurons: Possible relationships to aspects of peripheral neuropathic pain and paresthesias. Pain, 153 (9). pp. 1824-1836. (doi:10.1016/j.pain.2012.04.019) (KAR id:84445)

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https://doi.org/10.1016/j.pain.2012.04.019

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 heathypersensitivity/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-, Aδ-, and Aβ-nociceptors and cutaneous Aα/β-low-thresholdmechanoreceptors with ongoing/spontaneous firing; (b) spontaneous firing in C-nociceptors that originated peripherally; this was ata faster rate in modified-SNA than SNA; (c) decreased electricalthresholds in A-nociceptors after SNA; (d) hyperpolarised membrane potentials in A-nociceptors and Aα/-low-thresholdmechanoreceptors after SNA, but not C-nociceptors; (e) decreased somatic action potential rise times in C- and A-nociceptors, not Aα/β-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 Aα/β-low-threshold-mechanoreceptors to dysesthesias/paresthesias; and lowered A-nociceptor electrical thresholds to A-nociceptor sensitization, and greater evoked pain.

Item Type: Article
DOI/Identification number: 10.1016/j.pain.2012.04.019
Subjects: Q Science > QP Physiology (Living systems)
R Medicine > RC Internal medicine > RC321 Neuroscience. Biological psychiatry. Neuropsychiatry
Divisions: Divisions > Division of Natural Sciences > Medway School of Pharmacy
Depositing User: Stella Koutsikou
Date Deposited: 25 Nov 2020 12:44 UTC
Last Modified: 16 Feb 2021 14:16 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/84445 (The current URI for this page, for reference purposes)
Koutsikou, Stella: https://orcid.org/0000-0003-2933-3637
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