标题:Ca2+ influx mediates the TRPV4-NO pathway in neuropathic hyperalgesia following chronic compression of the dorsal root ganglion
作者:Wang, Jie; Wang, Xiao-Wei; Zhang, Yang; Yin, Cui-Ping; Yue, Shou-Wei
作者机构:[Wang, Jie; Zhang, Yang; Yin, Cui-Ping; Yue, Shou-Wei] Shandong Univ, Qilu Hosp, Dept Phys Med & Rehabil, Sch Med, Jinan 250012, Peoples R China.; [ 更多
通讯作者:Yue, SW
通讯作者地址:[Yue, SW]Shandong Univ, Qilu Hosp, Dept Phys Med & Rehabil, Sch Med, Jinan 250012, Peoples R China.
来源:NEUROSCIENCE LETTERS
出版年:2015
卷:588
页码:159-165
DOI:10.1016/j.neulet.2015.01.010
关键词:Nuclear factor-kappa B; Nitric oxide; TRPV4; Neuropathic hyperalgesia;; Calcium signalling
摘要:Chronic compression of the dorsal root ganglion (DRG) (CCD) in rats is a typical model of neuropathic pain. TRPV4 contributed to mechanical allodynia induced by the CCD model. Our previous study demonstrated that TRPV4 enhances neuropathic hyperalgesia through a NO-cGMP-PKG cascade. However, the underlying mechanism(s) is still largely unknown. Therefore, the aim of the present study was to test whether TRPV4-mediated Ca2+ influx is involved in the TRPV4-NO pathway. Regulation of intracellular calcium concentration by intrathecal injection of TRPV4-targeted siRNA significantly decreased the behavioural hyperalgesia, NF-kappa B activity, and NO content in CCD rats. Intraperitoneal (i.p.) injection of mibefradil significantly induced dose-dependent increases in the paw withdrawal latency (PWL) and mechanical withdrawal thresholds (MWT), as well as decreases in NF-KB activity and NO content in DRG of CCD rats. Moreover, pre-treatment with 4 alpha-PDD attenuated the suppressive effects of mibefradil on CCD-induced neuropathic hyperalgesia, NF-KB activity, and NO production. The data showed that TRPV4-mediated Ca2+ influx might be engaged in the TRPV4-NO pathway in neuropathic hyperalgesia in the CCD model. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
收录类别:SCOPUS;SCIE
WOS核心被引频次:7
Scopus被引频次:7
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84920943631&doi=10.1016%2fj.neulet.2015.01.010&partnerID=40&md5=1888f9ad7f328acfcefb38c11f3dd7d8
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