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学科主题: 基础医学
题名:
Suppression of KCNQ/M (Kv7) potassium channels in dorsal root ganglion neurons contributes to the development of bone cancer pain in a rat model
作者: Zheng, Qin1,2; Fang, Dong1,2; Liu, Min1,2; Cai, Jie1,2; Wan, You3,4; Han, Ji-Sheng1,2,3,4; Xing, Guo-Gang1,2,3,4
关键词: Bone cancer pain ; Dorsal root ganglion ; Hyperexcitability ; KCNQ channel ; M current ; Retigabine ; XE-991
刊名: PAIN
发表日期: 2013-03-01
DOI: 10.1016/j.pain.2012.12.005
卷: 154, 期:3, 页:434-448
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Anesthesiology ; Clinical Neurology ; Neurosciences
研究领域[WOS]: Anesthesiology ; Neurosciences & Neurology
关键词[WOS]: MEMBRANE-POTENTIAL OSCILLATIONS ; NR2B-CONTAINING NMDA RECEPTORS ; M-CURRENT MODULATORS ; SRC TYROSINE KINASE ; NEUROPATHIC PAIN ; K+ CHANNELS ; SENSORY NEURONS ; SYMPATHETIC NEURONS ; MEDIATED INHIBITION ; NERVE INJURY
英文摘要:

Bone cancer pain has a strong impact on the quality of life of patients, but is difficult to treat. Better understanding of the pathogenic mechanisms underlying bone cancer pain will likely lead to the development of more effective treatments. In the present study, we investigated whether inhibition of KCNQ/M channels contributed to the hyperexcitability of primary sensory neurons and to the pathogenesis of bone cancer pain. By using a rat model of bone cancer pain based on intratibial injection of MRMT-1 tumour cells, we documented a prominent decrease in expression of KCNQ2 and KCNQ3 proteins and a reduction of M-current density in small-sized dorsal root ganglia (DRG) neurons, which were associated with enhanced excitability of these DRG neurons and the hyperalgesic behaviours in bone cancer rats. Coincidently, we found that inhibition of KCNQ/M channels with XE-991 caused a robust increase in the excitability of small-sized DRG neurons and produced an obvious mechanical allodynia in normal rats. On the contrary, activation of the KCNQ/M channels with retigabine not only inhibited the hyperexcitability of these small DRG neurons, but also alleviated mechanical allodynia and thermal hyperalgesia in bone cancer rats, and all of these effects of retigabine could be blocked by KCNQ/M-channel antagonist XE-991. These results suggest that repression of KCNQ/M channels leads to the hyperexcitability of primary sensory neurons, which in turn causes bone cancer pain. Thus, suppression of KCNQ/M channels in primary DRG neurons plays a crucial role in the development of bone cancer pain. (C) 2012 International Association for the Study of Pain. Published by Elsevier B. V. All rights reserved.

语种: 英语
所属项目编号: 31171063 ; 81072951 ; 61027001 ; 7112079 ; 201302013 ; 2013CB531905
项目资助者: 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 Peoples Republic of China ; Ministry of Science and Technology of China
WOS记录号: WOS:000315299800018
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57104
Appears in Collections:基础医学院_神经生物学系_期刊论文

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作者单位: 1.Peking Univ, Neurosci Res Inst, Beijing 100191, Peoples R China
2.Peking Univ, Dept Neurobiol, Beijing 100191, Peoples R China
3.Minist Educ, Key Lab Neurosci, Beijing, Peoples R China
4.Minist Publ Hlth, Beijing, Peoples R China

Recommended Citation:
Zheng, Qin,Fang, Dong,Liu, Min,et al. Suppression of KCNQ/M (Kv7) potassium channels in dorsal root ganglion neurons contributes to the development of bone cancer pain in a rat model[J]. PAIN,2013,154(3):434-448.
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