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外周伤害感受通路上的 M 型 K 通道。

M-type K channels in peripheral nociceptive pathways.

机构信息

Department of Pharmacology, The Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Medical University, Shijiazhuang, China.

The Key Laboratory of New Drug Pharmacology and Toxicology, Shijiazhuang, Hebei Province, China.

出版信息

Br J Pharmacol. 2018 Jun;175(12):2158-2172. doi: 10.1111/bph.13978. Epub 2017 Sep 17.

DOI:10.1111/bph.13978
PMID:28800673
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5980636/
Abstract

UNLABELLED

Pathological pain is a hyperexcitability disorder. Since the excitability of a neuron is set and controlled by a complement of ion channels it expresses, in order to understand and treat pain, we need to develop a mechanistic insight into the key ion channels controlling excitability within the mammalian pain pathways and how these ion channels are regulated and modulated in various physiological and pathophysiological settings. In this review, we will discuss the emerging data on the expression in pain pathways, functional role and modulation of a family of voltage-gated K channels called 'M channels' (KCNQ, K 7). M channels are increasingly recognized as important players in controlling pain signalling, especially within the peripheral somatosensory system. We will also discuss the therapeutic potential of M channels as analgesic drug targets.

LINKED ARTICLES

This article is part of a themed section on Recent Advances in Targeting Ion Channels to Treat Chronic Pain. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc/.

摘要

未加标签

病理性疼痛是一种过度兴奋障碍。由于神经元的兴奋性由其表达的一组离子通道设定和控制,因此,为了理解和治疗疼痛,我们需要深入了解控制哺乳动物疼痛途径中兴奋性的关键离子通道,以及这些离子通道在各种生理和病理生理状态下是如何被调节和调制的。在这篇综述中,我们将讨论在疼痛途径中表达、功能作用和调节越来越被认为是控制疼痛信号的重要参与者的电压门控钾通道家族“M 通道”(KCNQ、K7)的新兴数据。我们还将讨论 M 通道作为镇痛药物靶点的治疗潜力。

相关文章

本文是一个主题部分的一部分,主题是“靶向离子通道治疗慢性疼痛的最新进展”。要查看本节中的其他文章,请访问 http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.12/issuetoc/。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/cd1c0411b824/BPH-175-2158-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/8dc12840a77d/BPH-175-2158-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/35903a5f9bbe/BPH-175-2158-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/075dc3f5168c/BPH-175-2158-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/cd1c0411b824/BPH-175-2158-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/8dc12840a77d/BPH-175-2158-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/35903a5f9bbe/BPH-175-2158-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/075dc3f5168c/BPH-175-2158-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79c3/5980636/cd1c0411b824/BPH-175-2158-g004.jpg

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