Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury

Calvo, Margarita, Richards, Natalie, Schmid, Annina B., Barroso, Alejandro, Zhu, Lan, Ivulic, Dinka, Zhu, Ning, Anwandter, Philipp, Bhat, Manzoor A., Court, Felipe A., McMahon, Stephen B. and Bennett, David L. H. (2016) Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury. eLife, 5 . doi:10.7554/eLife.12661


Author Calvo, Margarita
Richards, Natalie
Schmid, Annina B.
Barroso, Alejandro
Zhu, Lan
Ivulic, Dinka
Zhu, Ning
Anwandter, Philipp
Bhat, Manzoor A.
Court, Felipe A.
McMahon, Stephen B.
Bennett, David L. H.
Title Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury
Journal name eLife   Check publisher's open access policy
ISSN 2050-084X
Publication date 2016-04-01
Year available 2016
Sub-type Article (original research)
DOI 10.7554/eLife.12661
Open Access Status DOI
Volume 5
Total pages 26
Place of publication Cambridge, United Kingdom
Publisher eLife Sciences Publications
Collection year 2017
Language eng
Abstract Neuropathic pain following peripheral nerve injury is associated with hyperexcitability in damaged myelinated sensory axons, which begins to normalise over time. We investigated the composition and distribution of Shaker-Type-Potassium channels (Kv1 channels) within the nodal complex of myelinated axons following injury. At the neuroma that forms after damage, expression of Kv1.1 and 1.2 (normally localised to the juxtaparanode) was markedly decreased. In contrast Kv1.4 and 1.6, which were hardly detectable in the naïve state, showed increased expression within juxtaparanodes and paranodes following injury, both in rats and humans. Within the dorsal root (a site remote from injury) we noted a redistribution of Kv1-Channels towards the paranode. Blockade of Kv1 channels with α-DTX after injury reinstated hyperexcitability of A-fibre axons and enhanced mechanosensitivity. Changes in the molecular composition and distribution of axonal Kv1 channels, therefore represents a protective mechanism to suppress the hyperexcitability of myelinated sensory axons that follows nerve injury.
Keyword Myelinated axons
Hyperexcitability
Neuropathic pain
Peripheral nerve injury
Kv1 channels
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
School of Health and Rehabilitation Sciences Publications
 
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