Cargando…

Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats

BACKGROUND: A previous study found that brain natriuretic peptide (BNP) inhibited inflammatory pain via activating its receptor natriuretic peptide receptor A (NPRA) in nociceptive sensory neurons. A recent study found that functional NPRA is expressed in almost all the trigeminal ganglion (TG) neur...

Descripción completa

Detalles Bibliográficos
Autores principales: Li, Zheng-Wei, Wu, Bin, Ye, Pin, Tan, Zhi-Yong, Ji, Yong-Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Milan 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5042912/
https://www.ncbi.nlm.nih.gov/pubmed/27687165
http://dx.doi.org/10.1186/s10194-016-0685-y
_version_ 1782456664192974848
author Li, Zheng-Wei
Wu, Bin
Ye, Pin
Tan, Zhi-Yong
Ji, Yong-Hua
author_facet Li, Zheng-Wei
Wu, Bin
Ye, Pin
Tan, Zhi-Yong
Ji, Yong-Hua
author_sort Li, Zheng-Wei
collection PubMed
description BACKGROUND: A previous study found that brain natriuretic peptide (BNP) inhibited inflammatory pain via activating its receptor natriuretic peptide receptor A (NPRA) in nociceptive sensory neurons. A recent study found that functional NPRA is expressed in almost all the trigeminal ganglion (TG) neurons at membrane level suggesting a potentially important role for BNP in migraine pathophysiology. METHODS: An inflammatory pain model was produced by subcutaneous injection of BmK I, a sodium channel-specific modulator from venom of Chinese scorpion Buthus martensi Karsch. Quantitative PCR, Western Blot, and immunohistochemistry were used to detect mRNA and protein expression of BNP and NPRA in dorsal root ganglion (DRG) and dorsal horn of spinal cord. Whole-cell patch clamping experiments were conducted to record large-conductance Ca(2+)-activated K(+) (BK(Ca)) currents of membrane excitability of DRG neurons. Spontaneous and evoked pain behaviors were examined. RESULTS: The mRNA and protein expression of BNP and NPRA was up-regulated in DRG and dorsal horn of spinal cord after BmK I injection. The BNP and NPRA was preferentially expressed in small-sized DRG neurons among which BNP was expressed in both CGRP-positive and IB4-positive neurons while NPRA was preferentially expressed in CGRP-positive neurons. BNP increased the open probability of BK(Ca) channels and suppressed the membrane excitability of small-sized DRG neurons. Intrathecal injection of BNP significantly inhibited BmK-induced pain behaviors including both spontaneous and evoked pain behaviors. CONCLUSIONS: These results suggested that BNP might play an important role as an endogenous pain reliever in BmK I-induced inflammatory pain condition. It is also suggested that BNP might play a similar role in other pathophysiological pain conditions including migraine.
format Online
Article
Text
id pubmed-5042912
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Springer Milan
record_format MEDLINE/PubMed
spelling pubmed-50429122016-10-03 Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats Li, Zheng-Wei Wu, Bin Ye, Pin Tan, Zhi-Yong Ji, Yong-Hua J Headache Pain Research Article BACKGROUND: A previous study found that brain natriuretic peptide (BNP) inhibited inflammatory pain via activating its receptor natriuretic peptide receptor A (NPRA) in nociceptive sensory neurons. A recent study found that functional NPRA is expressed in almost all the trigeminal ganglion (TG) neurons at membrane level suggesting a potentially important role for BNP in migraine pathophysiology. METHODS: An inflammatory pain model was produced by subcutaneous injection of BmK I, a sodium channel-specific modulator from venom of Chinese scorpion Buthus martensi Karsch. Quantitative PCR, Western Blot, and immunohistochemistry were used to detect mRNA and protein expression of BNP and NPRA in dorsal root ganglion (DRG) and dorsal horn of spinal cord. Whole-cell patch clamping experiments were conducted to record large-conductance Ca(2+)-activated K(+) (BK(Ca)) currents of membrane excitability of DRG neurons. Spontaneous and evoked pain behaviors were examined. RESULTS: The mRNA and protein expression of BNP and NPRA was up-regulated in DRG and dorsal horn of spinal cord after BmK I injection. The BNP and NPRA was preferentially expressed in small-sized DRG neurons among which BNP was expressed in both CGRP-positive and IB4-positive neurons while NPRA was preferentially expressed in CGRP-positive neurons. BNP increased the open probability of BK(Ca) channels and suppressed the membrane excitability of small-sized DRG neurons. Intrathecal injection of BNP significantly inhibited BmK-induced pain behaviors including both spontaneous and evoked pain behaviors. CONCLUSIONS: These results suggested that BNP might play an important role as an endogenous pain reliever in BmK I-induced inflammatory pain condition. It is also suggested that BNP might play a similar role in other pathophysiological pain conditions including migraine. Springer Milan 2016-09-29 /pmc/articles/PMC5042912/ /pubmed/27687165 http://dx.doi.org/10.1186/s10194-016-0685-y Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Research Article
Li, Zheng-Wei
Wu, Bin
Ye, Pin
Tan, Zhi-Yong
Ji, Yong-Hua
Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title_full Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title_fullStr Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title_full_unstemmed Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title_short Brain natriuretic peptide suppresses pain induced by BmK I, a sodium channel-specific modulator, in rats
title_sort brain natriuretic peptide suppresses pain induced by bmk i, a sodium channel-specific modulator, in rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5042912/
https://www.ncbi.nlm.nih.gov/pubmed/27687165
http://dx.doi.org/10.1186/s10194-016-0685-y
work_keys_str_mv AT lizhengwei brainnatriureticpeptidesuppressespaininducedbybmkiasodiumchannelspecificmodulatorinrats
AT wubin brainnatriureticpeptidesuppressespaininducedbybmkiasodiumchannelspecificmodulatorinrats
AT yepin brainnatriureticpeptidesuppressespaininducedbybmkiasodiumchannelspecificmodulatorinrats
AT tanzhiyong brainnatriureticpeptidesuppressespaininducedbybmkiasodiumchannelspecificmodulatorinrats
AT jiyonghua brainnatriureticpeptidesuppressespaininducedbybmkiasodiumchannelspecificmodulatorinrats