IR@PKUHSC  > 北京大学基础医学院  > 神经生物学系
学科主题基础医学
Functional Upregulation of Nav1.8 Sodium Channels on the Membrane of Dorsal Root Ganglia Neurons Contributes to the Development of Cancer-Induced Bone Pain
Liu, Xiao-Dan1,2; Yang, Jing-Jing1; Fang, Dong1; Cai, Jie1,2; Wan, You2; Xing, Guo-Gang1,2,3,4
刊名PLOS ONE
2014-12-11
DOI10.1371/journal.pone.0114623
9期:12
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]ACTION-POTENTIAL ELECTROGENESIS ; NR2B-CONTAINING NMDA RECEPTORS ; PRIMARY AFFERENT NEURONS ; RESISTANT NA+ CURRENT ; NEUROPATHIC PAIN ; INFLAMMATORY PAIN ; SENSORY NEURONS ; DRG NEURONS ; RAT MODEL ; EXPRESSION
英文摘要

We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. We speculate that the Nav1.8 sodium channel is a potential candidate responsible for the enhanced excitability of DRG neurons in rats with bone cancer pain. Here, using electrophysiology, Western blot and behavior assays, we documented that the current density of TTX-R sodium channels, especially the Nav1.8 channel, increased significantly in DRG neurons of rats with cancer-induced bone pain. This increase may be due to an increased expression of Nav1.8 on the membrane of DRG neurons. Accordantly, blockade of Nav1.8 sodium channels by its selective blocker A-803467 significantly alleviated the cancer-induced mechanical allodynia and thermal hyperalgesia in rats. Taken together, these results suggest that functional upregulation of Nav1.8 channels on the membrane of DRG neurons contributes to the development of cancer-induced bone pain.

语种英语
WOS记录号WOS:000347146700034
项目编号81371237 ; 31171063 ; 81072951 ; 7112079 ; 201302013-01 ; 2013CB531905
资助机构National Natural Science Foundation of China ; Beijing Natural Science Foundation ; special foundation for public welfare profession scientific research program from Ministry of Health of the People&prime ; s Republic of China ; "973" Program of the Ministry of Science and Technology of China
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57138
专题北京大学基础医学院_神经生物学系
北京大学基础医学院
北京大学口腔医学院_综合治疗科
作者单位1.Peking Univ, Neurosci Res Inst, Beijing 100871, Peoples R China
2.Minist Educ, Key Lab Neurosci, Beijing, Peoples R China
3.Minist Hlth, Beijing, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Neurobiol, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Liu, Xiao-Dan,Yang, Jing-Jing,Fang, Dong,et al. Functional Upregulation of Nav1.8 Sodium Channels on the Membrane of Dorsal Root Ganglia Neurons Contributes to the Development of Cancer-Induced Bone Pain[J]. PLOS ONE,2014,9(12).
APA Liu, Xiao-Dan,Yang, Jing-Jing,Fang, Dong,Cai, Jie,Wan, You,&Xing, Guo-Gang.(2014).Functional Upregulation of Nav1.8 Sodium Channels on the Membrane of Dorsal Root Ganglia Neurons Contributes to the Development of Cancer-Induced Bone Pain.PLOS ONE,9(12).
MLA Liu, Xiao-Dan,et al."Functional Upregulation of Nav1.8 Sodium Channels on the Membrane of Dorsal Root Ganglia Neurons Contributes to the Development of Cancer-Induced Bone Pain".PLOS ONE 9.12(2014).
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
Functional Upregulat(953KB)期刊论文出版稿开放获取CC BY-NC-SA浏览 请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Liu, Xiao-Dan]的文章
[Yang, Jing-Jing]的文章
[Fang, Dong]的文章
百度学术
百度学术中相似的文章
[Liu, Xiao-Dan]的文章
[Yang, Jing-Jing]的文章
[Fang, Dong]的文章
必应学术
必应学术中相似的文章
[Liu, Xiao-Dan]的文章
[Yang, Jing-Jing]的文章
[Fang, Dong]的文章
相关权益政策
暂无数据
收藏/分享
文件名: Functional Upregulation of Nav1.8 Sodium Channels on the Membrane of Dorsal Root Ganglia Neurons Contributes to the Development of Cancer-Induced Bone Pain.pdf
格式: Adobe PDF
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。