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Kv3.4 channel function and dysfunction in nociceptors

Recently, we reported the isolation of the Kv3.4 current in dorsal root ganglion (DRG) neurons and described dysregulation of this current in a spinal cord injury (SCI) model of chronic pain. These studies strongly suggest that rat Kv3.4 channels are major regulators of excitability in DRG neurons f...

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Detalles Bibliográficos
Autores principales: Ritter, David M, Zemel, Benjamin M, Lepore, Angelo C, Covarrubias, Manuel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594523/
https://www.ncbi.nlm.nih.gov/pubmed/26039360
http://dx.doi.org/10.1080/19336950.2015.1056949
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author Ritter, David M
Zemel, Benjamin M
Lepore, Angelo C
Covarrubias, Manuel
author_facet Ritter, David M
Zemel, Benjamin M
Lepore, Angelo C
Covarrubias, Manuel
author_sort Ritter, David M
collection PubMed
description Recently, we reported the isolation of the Kv3.4 current in dorsal root ganglion (DRG) neurons and described dysregulation of this current in a spinal cord injury (SCI) model of chronic pain. These studies strongly suggest that rat Kv3.4 channels are major regulators of excitability in DRG neurons from pups and adult females, where they help determine action potential (AP) repolarization and spiking properties. Here, we characterized the Kv3.4 current in rat DRG neurons from adult males and show that it transfers 40–70% of the total repolarizing charge during the AP across all ages and sexes. Following SCI, we also found remodeling of the repolarizing currents during the AP. In the light of these studies, homomeric Kv3.4 channels expressed in DRG nociceptors are emerging novel targets that may help develop new approaches to treat neuropathic pain.
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spelling pubmed-45945232016-02-03 Kv3.4 channel function and dysfunction in nociceptors Ritter, David M Zemel, Benjamin M Lepore, Angelo C Covarrubias, Manuel Channels (Austin) Article Addenda Recently, we reported the isolation of the Kv3.4 current in dorsal root ganglion (DRG) neurons and described dysregulation of this current in a spinal cord injury (SCI) model of chronic pain. These studies strongly suggest that rat Kv3.4 channels are major regulators of excitability in DRG neurons from pups and adult females, where they help determine action potential (AP) repolarization and spiking properties. Here, we characterized the Kv3.4 current in rat DRG neurons from adult males and show that it transfers 40–70% of the total repolarizing charge during the AP across all ages and sexes. Following SCI, we also found remodeling of the repolarizing currents during the AP. In the light of these studies, homomeric Kv3.4 channels expressed in DRG nociceptors are emerging novel targets that may help develop new approaches to treat neuropathic pain. Taylor & Francis 2015-06-03 /pmc/articles/PMC4594523/ /pubmed/26039360 http://dx.doi.org/10.1080/19336950.2015.1056949 Text en © 2015 The Author(s). Published with license by Taylor & Francis Group, LLC http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.
spellingShingle Article Addenda
Ritter, David M
Zemel, Benjamin M
Lepore, Angelo C
Covarrubias, Manuel
Kv3.4 channel function and dysfunction in nociceptors
title Kv3.4 channel function and dysfunction in nociceptors
title_full Kv3.4 channel function and dysfunction in nociceptors
title_fullStr Kv3.4 channel function and dysfunction in nociceptors
title_full_unstemmed Kv3.4 channel function and dysfunction in nociceptors
title_short Kv3.4 channel function and dysfunction in nociceptors
title_sort kv3.4 channel function and dysfunction in nociceptors
topic Article Addenda
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4594523/
https://www.ncbi.nlm.nih.gov/pubmed/26039360
http://dx.doi.org/10.1080/19336950.2015.1056949
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