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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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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. |
format | Online Article Text |
id | pubmed-4083869 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
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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