Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia

Background C fibre hyperexcitability is fundamental to chronic pain development in humans and rodents; therefore, peripheral sensory neuronal sensitization plays a role in the development of mechanical hyperalgesia. However, the axonal properties and underlying mechanisms that are associated to t...

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Main Author: Hulse, Richard P.
Format: Article
Published: Wiley 2015
Online Access:https://eprints.nottingham.ac.uk/36748/
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author Hulse, Richard P.
author_facet Hulse, Richard P.
author_sort Hulse, Richard P.
building Nottingham Research Data Repository
collection Online Access
description Background C fibre hyperexcitability is fundamental to chronic pain development in humans and rodents; therefore, peripheral sensory neuronal sensitization plays a role in the development of mechanical hyperalgesia. However, the axonal properties and underlying mechanisms that are associated to these chronic pain states still require investigation. Methods Teased fibre electrophysiology of the saphenous nerve was used to identify C fibres in naïve and nerve-injured rats. C fibres were identified using electrical stimulation which further provided conduction velocity slowing profiles. From these nerve filaments evoked responses to mechanical stimuli were recorded. Vehicle or galanin were applied directly to the saphenous nerve trunk prior to stimulation. Results Increased levels of mechanically evoked activity in mechano-sensitive C fibres was associated to reduced conduction failure, enhanced conduction velocity latency recovery and reduced conduction velocity slowing. Mechanical hyperalgesia developed in nerve-injured animals in which mechano-sensitive C fibres demonstrated increased mechanically evoked responses and reduced rate of adaptation. Mechano-sensitive C fibres in nerve-injured animals had reduced levels of conduction velocity slowing, enhanced rate of conduction velocity recovery and reduced firing frequency failure versus naïve animals; all hallmarks of enhanced sensory neuronal excitability. Directly applying the antinociceptive agent galanin to the saphenous nerve trunk in naive animals led to increased conduction failure, reduced latency recovery rate and increased levels of conduction velocity slowing. Discussion Nerve injury-induced enhanced neural responses to mechanical stimulation are associated to defined parameters setout by conduction velocity slowing, mediated via axonal processing. Application of galanin inhibits axonal excitability.
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spelling nottingham-367482020-05-04T17:20:37Z https://eprints.nottingham.ac.uk/36748/ Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia Hulse, Richard P. Background C fibre hyperexcitability is fundamental to chronic pain development in humans and rodents; therefore, peripheral sensory neuronal sensitization plays a role in the development of mechanical hyperalgesia. However, the axonal properties and underlying mechanisms that are associated to these chronic pain states still require investigation. Methods Teased fibre electrophysiology of the saphenous nerve was used to identify C fibres in naïve and nerve-injured rats. C fibres were identified using electrical stimulation which further provided conduction velocity slowing profiles. From these nerve filaments evoked responses to mechanical stimuli were recorded. Vehicle or galanin were applied directly to the saphenous nerve trunk prior to stimulation. Results Increased levels of mechanically evoked activity in mechano-sensitive C fibres was associated to reduced conduction failure, enhanced conduction velocity latency recovery and reduced conduction velocity slowing. Mechanical hyperalgesia developed in nerve-injured animals in which mechano-sensitive C fibres demonstrated increased mechanically evoked responses and reduced rate of adaptation. Mechano-sensitive C fibres in nerve-injured animals had reduced levels of conduction velocity slowing, enhanced rate of conduction velocity recovery and reduced firing frequency failure versus naïve animals; all hallmarks of enhanced sensory neuronal excitability. Directly applying the antinociceptive agent galanin to the saphenous nerve trunk in naive animals led to increased conduction failure, reduced latency recovery rate and increased levels of conduction velocity slowing. Discussion Nerve injury-induced enhanced neural responses to mechanical stimulation are associated to defined parameters setout by conduction velocity slowing, mediated via axonal processing. Application of galanin inhibits axonal excitability. Wiley 2015-10-02 Article PeerReviewed Hulse, Richard P. (2015) Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia. European Journal of Pain, 20 (4). pp. 615-625. ISSN 1532-2149 http://onlinelibrary.wiley.com/doi/10.1002/ejp.779/abstract;jsessionid=728A7688A7B4C2BD341AD0CCAACBEB17.f02t01 doi:10.1002/ejp.779 doi:10.1002/ejp.779
spellingShingle Hulse, Richard P.
Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title_full Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title_fullStr Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title_full_unstemmed Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title_short Identification of mechano-sensitive C fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
title_sort identification of mechano-sensitive c fibre sensitization and contribution to nerve injury-induced mechanical hyperalgesia
url https://eprints.nottingham.ac.uk/36748/
https://eprints.nottingham.ac.uk/36748/
https://eprints.nottingham.ac.uk/36748/