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Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia

BACKGROUND: Tissue acidosis is effective in causing chronic muscle pain. However, how muscle nociceptors contribute to the transition from acute to chronic pain is largely unknown. RESULTS: Here we showed that a single intramuscular acid injection induced a priming effect on muscle nociceptors of mi...

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Autores principales: Chen, Wei-Nan, Lee, Cheng-Han, Lin, Shing-Hong, Wong, Chia-Wen, Sun, Wei-Hsin, Wood, John N, Chen, Chih-Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4083869/
https://www.ncbi.nlm.nih.gov/pubmed/24957987
http://dx.doi.org/10.1186/1744-8069-10-40
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author Chen, Wei-Nan
Lee, Cheng-Han
Lin, Shing-Hong
Wong, Chia-Wen
Sun, Wei-Hsin
Wood, John N
Chen, Chih-Cheng
author_facet Chen, Wei-Nan
Lee, Cheng-Han
Lin, Shing-Hong
Wong, Chia-Wen
Sun, Wei-Hsin
Wood, John N
Chen, Chih-Cheng
author_sort Chen, Wei-Nan
collection PubMed
description BACKGROUND: Tissue acidosis is effective in causing chronic muscle pain. However, how muscle nociceptors contribute to the transition from acute to chronic pain is largely unknown. RESULTS: Here we showed that a single intramuscular acid injection induced a priming effect on muscle nociceptors of mice. The primed muscle nociceptors were plastic and permitted the development of long-lasting chronic hyperalgesia induced by a second acid insult. The plastic changes of muscle nociceptors were modality-specific and required the activation of acid-sensing ion channel 3 (ASIC3) or transient receptor potential cation channel V1 (TRPV1). Activation of ASIC3 was associated with increased activity of tetrodotoxin (TTX)-sensitive voltage-gated sodium channels but not protein kinase Cϵ (PKCϵ) in isolectin B4 (IB4)-negative muscle nociceptors. In contrast, increased activity of TTX-resistant voltage-gated sodium channels with ASIC3 or TRPV1 activation in Na(V)1.8-positive muscle nociceptors was required for the development of chronic hyperalgesia. Accordingly, compared to wild type mice, Na(V)1.8-null mice showed briefer acid-induced hyperalgesia (5 days vs. >27 days). CONCLUSION: ASIC3 activation may manifest a new type of nociceptor priming in IB4-negative muscle nociceptors. The activation of ASIC3 and TRPV1 as well as enhanced Na(V)1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain.
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spelling pubmed-40838692014-07-08 Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia Chen, Wei-Nan Lee, Cheng-Han Lin, Shing-Hong Wong, Chia-Wen Sun, Wei-Hsin Wood, John N Chen, Chih-Cheng Mol Pain Research BACKGROUND: Tissue acidosis is effective in causing chronic muscle pain. However, how muscle nociceptors contribute to the transition from acute to chronic pain is largely unknown. RESULTS: Here we showed that a single intramuscular acid injection induced a priming effect on muscle nociceptors of mice. The primed muscle nociceptors were plastic and permitted the development of long-lasting chronic hyperalgesia induced by a second acid insult. The plastic changes of muscle nociceptors were modality-specific and required the activation of acid-sensing ion channel 3 (ASIC3) or transient receptor potential cation channel V1 (TRPV1). Activation of ASIC3 was associated with increased activity of tetrodotoxin (TTX)-sensitive voltage-gated sodium channels but not protein kinase Cϵ (PKCϵ) in isolectin B4 (IB4)-negative muscle nociceptors. In contrast, increased activity of TTX-resistant voltage-gated sodium channels with ASIC3 or TRPV1 activation in Na(V)1.8-positive muscle nociceptors was required for the development of chronic hyperalgesia. Accordingly, compared to wild type mice, Na(V)1.8-null mice showed briefer acid-induced hyperalgesia (5 days vs. >27 days). CONCLUSION: ASIC3 activation may manifest a new type of nociceptor priming in IB4-negative muscle nociceptors. The activation of ASIC3 and TRPV1 as well as enhanced Na(V)1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain. BioMed Central 2014-06-23 /pmc/articles/PMC4083869/ /pubmed/24957987 http://dx.doi.org/10.1186/1744-8069-10-40 Text en Copyright © 2014 Chen et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Chen, Wei-Nan
Lee, Cheng-Han
Lin, Shing-Hong
Wong, Chia-Wen
Sun, Wei-Hsin
Wood, John N
Chen, Chih-Cheng
Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title_full Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title_fullStr Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title_full_unstemmed Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title_short Roles of ASIC3, TRPV1, and Na(V)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
title_sort roles of asic3, trpv1, and na(v)1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4083869/
https://www.ncbi.nlm.nih.gov/pubmed/24957987
http://dx.doi.org/10.1186/1744-8069-10-40
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