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Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat
Reactive oxygen species (ROS) are generated in nociceptive pathways in response to inflammation and injury. ROS are accumulated within the sensory ganglia following peripheral inflammation, but the functional role of intraganlionic ROS in inflammatory pain is not clearly understood. The aims of this...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10261988/ https://www.ncbi.nlm.nih.gov/pubmed/37325677 http://dx.doi.org/10.3389/fpain.2023.1204057 |
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author | Zhang, Youping Asgar, Jamila Shou, Huizhong Pak, Joshua Da Silva, Joyce Teixeira Ro, Jin Y. |
author_facet | Zhang, Youping Asgar, Jamila Shou, Huizhong Pak, Joshua Da Silva, Joyce Teixeira Ro, Jin Y. |
author_sort | Zhang, Youping |
collection | PubMed |
description | Reactive oxygen species (ROS) are generated in nociceptive pathways in response to inflammation and injury. ROS are accumulated within the sensory ganglia following peripheral inflammation, but the functional role of intraganlionic ROS in inflammatory pain is not clearly understood. The aims of this study were to investigate whether peripheral inflammation leads to prolonged ROS accumulation within the trigeminal ganglia (TG), whether intraganglionic ROS mediate pain hypersensitivity via activation of TRPA1, and whether TRPA1 expression is upregulated in TG during inflammatory conditions by ROS. We demonstrated that peripheral inflammation causes excess ROS production within TG during the period when inflammatory mechanical hyperalgesia is most prominent. Additionally, scavenging intraganglionic ROS attenuated inflammatory mechanical hyperalgesia and a pharmacological blockade of TRPA1 localized within TG also mitigated inflammatory mechanical hyperalgesia. Interestingly, exogenous administration of ROS into TG elicited mechanical hyperalgesia and spontaneous pain-like responses via TRPA1, and intraganglionic ROS induced TRPA1 upregulation in TG. These results collectively suggest that ROS accumulation in TG during peripheral inflammation contributes to pain and hyperalgesia in a TRPA1 dependent manner, and that ROS further exacerbate pathological pain responses by upregulating TRPA1 expression. Therefore, any conditions that exacerbate ROS accumulation within somatic sensory ganglia can aggravate pain responses and treatments reducing ganglionic ROS may help alleviate inflammatory pain. |
format | Online Article Text |
id | pubmed-10261988 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-102619882023-06-15 Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat Zhang, Youping Asgar, Jamila Shou, Huizhong Pak, Joshua Da Silva, Joyce Teixeira Ro, Jin Y. Front Pain Res (Lausanne) Pain Research Reactive oxygen species (ROS) are generated in nociceptive pathways in response to inflammation and injury. ROS are accumulated within the sensory ganglia following peripheral inflammation, but the functional role of intraganlionic ROS in inflammatory pain is not clearly understood. The aims of this study were to investigate whether peripheral inflammation leads to prolonged ROS accumulation within the trigeminal ganglia (TG), whether intraganglionic ROS mediate pain hypersensitivity via activation of TRPA1, and whether TRPA1 expression is upregulated in TG during inflammatory conditions by ROS. We demonstrated that peripheral inflammation causes excess ROS production within TG during the period when inflammatory mechanical hyperalgesia is most prominent. Additionally, scavenging intraganglionic ROS attenuated inflammatory mechanical hyperalgesia and a pharmacological blockade of TRPA1 localized within TG also mitigated inflammatory mechanical hyperalgesia. Interestingly, exogenous administration of ROS into TG elicited mechanical hyperalgesia and spontaneous pain-like responses via TRPA1, and intraganglionic ROS induced TRPA1 upregulation in TG. These results collectively suggest that ROS accumulation in TG during peripheral inflammation contributes to pain and hyperalgesia in a TRPA1 dependent manner, and that ROS further exacerbate pathological pain responses by upregulating TRPA1 expression. Therefore, any conditions that exacerbate ROS accumulation within somatic sensory ganglia can aggravate pain responses and treatments reducing ganglionic ROS may help alleviate inflammatory pain. Frontiers Media S.A. 2023-05-30 /pmc/articles/PMC10261988/ /pubmed/37325677 http://dx.doi.org/10.3389/fpain.2023.1204057 Text en © 2023 Zhang, Asgar, Shou, Pak, Da Silva and Ro. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) (https://creativecommons.org/licenses/by/4.0/) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Pain Research Zhang, Youping Asgar, Jamila Shou, Huizhong Pak, Joshua Da Silva, Joyce Teixeira Ro, Jin Y. Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title | Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title_full | Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title_fullStr | Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title_full_unstemmed | Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title_short | Intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through TRPA1 in the rat |
title_sort | intraganglionic reactive oxygen species mediate inflammatory pain and hyperalgesia through trpa1 in the rat |
topic | Pain Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10261988/ https://www.ncbi.nlm.nih.gov/pubmed/37325677 http://dx.doi.org/10.3389/fpain.2023.1204057 |
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