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Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint

BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception. However, the role for H(2)S in nociceptive processing in trigeminal ganglion (TG) neuron remains unkn...

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Autores principales: Miao, Xiuhua, Meng, Xiaowen, Wu, Geping, Ju, Zhong, Zhang, Hong-Hong, Hu, Shufen, Xu, Guang-Yin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917612/
https://www.ncbi.nlm.nih.gov/pubmed/24490955
http://dx.doi.org/10.1186/1744-8069-10-9
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author Miao, Xiuhua
Meng, Xiaowen
Wu, Geping
Ju, Zhong
Zhang, Hong-Hong
Hu, Shufen
Xu, Guang-Yin
author_facet Miao, Xiuhua
Meng, Xiaowen
Wu, Geping
Ju, Zhong
Zhang, Hong-Hong
Hu, Shufen
Xu, Guang-Yin
author_sort Miao, Xiuhua
collection PubMed
description BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception. However, the role for H(2)S in nociceptive processing in trigeminal ganglion (TG) neuron remains unknown. The aim of this study was designed to investigate whether endogenous H(2)S synthesizing enzyme cystathionine-β-synthetase (CBS) plays a role in inflammatory pain in temporomandibular joint (TMJ). METHODS: TMJ inflammatory pain was induced by injection of complete Freund’s adjuvant (CFA) into TMJ of adult male rats. Von Frey filaments were used to examine pain behavioral responses in rats following injection of CFA or normal saline (NS). Whole cell patch clamp recordings were employed on acutely isolated TG neurons from rats 2 days after CFA injection. Western blot analysis was carried out to measure protein expression in TGs. RESULTS: Injection of CFA into TMJ produced a time dependent hyperalgesia as evidenced by reduced escape threshold in rats responding to VFF stimulation. The reduced escape threshold was partially reversed by injection of O-(Carboxymethyl) hydroxylamine hemihydrochloride (AOAA), an inhibitor for CBS, in a dose-dependent manner. CFA injection led to a marked upregulation of CBS expression when compared with age-matched controls. CFA injection enhanced neuronal excitability as evidenced by depolarization of resting membrane potentials, reduction in rheobase, and an increase in number of action potentials evoked by 2 and 3 times rheobase current stimulation and by a ramp current stimulation of TG neurons innervating the TMJ area. CFA injection also led to a reduction of I(K) but not I(A) current density of TG neurons. Application of AOAA in TMJ area reduced the production of H(2)S in TGs and reversed the enhanced neural hyperexcitability and increased the I(K) currents of TG neurons. CONCLUSION: These data together with our previous report indicate that endogenous H(2)S generating enzyme CBS plays an important role in TMJ inflammation, which is likely mediated by inhibition of I(K) currents, thus identifying a specific molecular mechanism underlying pain and sensitization in TMJ inflammation.
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spelling pubmed-39176122014-02-08 Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint Miao, Xiuhua Meng, Xiaowen Wu, Geping Ju, Zhong Zhang, Hong-Hong Hu, Shufen Xu, Guang-Yin Mol Pain Research BACKGROUND: Hydrogen sulfide (H(2)S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception. However, the role for H(2)S in nociceptive processing in trigeminal ganglion (TG) neuron remains unknown. The aim of this study was designed to investigate whether endogenous H(2)S synthesizing enzyme cystathionine-β-synthetase (CBS) plays a role in inflammatory pain in temporomandibular joint (TMJ). METHODS: TMJ inflammatory pain was induced by injection of complete Freund’s adjuvant (CFA) into TMJ of adult male rats. Von Frey filaments were used to examine pain behavioral responses in rats following injection of CFA or normal saline (NS). Whole cell patch clamp recordings were employed on acutely isolated TG neurons from rats 2 days after CFA injection. Western blot analysis was carried out to measure protein expression in TGs. RESULTS: Injection of CFA into TMJ produced a time dependent hyperalgesia as evidenced by reduced escape threshold in rats responding to VFF stimulation. The reduced escape threshold was partially reversed by injection of O-(Carboxymethyl) hydroxylamine hemihydrochloride (AOAA), an inhibitor for CBS, in a dose-dependent manner. CFA injection led to a marked upregulation of CBS expression when compared with age-matched controls. CFA injection enhanced neuronal excitability as evidenced by depolarization of resting membrane potentials, reduction in rheobase, and an increase in number of action potentials evoked by 2 and 3 times rheobase current stimulation and by a ramp current stimulation of TG neurons innervating the TMJ area. CFA injection also led to a reduction of I(K) but not I(A) current density of TG neurons. Application of AOAA in TMJ area reduced the production of H(2)S in TGs and reversed the enhanced neural hyperexcitability and increased the I(K) currents of TG neurons. CONCLUSION: These data together with our previous report indicate that endogenous H(2)S generating enzyme CBS plays an important role in TMJ inflammation, which is likely mediated by inhibition of I(K) currents, thus identifying a specific molecular mechanism underlying pain and sensitization in TMJ inflammation. BioMed Central 2014-02-03 /pmc/articles/PMC3917612/ /pubmed/24490955 http://dx.doi.org/10.1186/1744-8069-10-9 Text en Copyright © 2014 Miao et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), 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
Miao, Xiuhua
Meng, Xiaowen
Wu, Geping
Ju, Zhong
Zhang, Hong-Hong
Hu, Shufen
Xu, Guang-Yin
Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title_full Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title_fullStr Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title_full_unstemmed Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title_short Upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
title_sort upregulation of cystathionine-β-synthetase expression contributes to inflammatory pain in rat temporomandibular joint
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917612/
https://www.ncbi.nlm.nih.gov/pubmed/24490955
http://dx.doi.org/10.1186/1744-8069-10-9
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