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学科主题基础医学
Visceral hyperalgesia induced by forebrain-specific suppression of native Kv7/KCNQ/M-current in mice
Bi, Yeping1; Chen, Hui1; Su, Jun1; Cao, Xu1; Bian, Xiling1; Wang, KeWei1,2
关键词forebrain retigabine XE-991 capsaicin acetic acid c-Fos somatosensory cortex
刊名MOLECULAR PAIN
2011-10-26
DOI10.1186/1744-8069-7-84
7期:1
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]DEPENDENT PROTEIN-KINASE ; MOUSE-BRAIN ; RAT-BRAIN ; M-CHANNEL ; CENTRAL SENSITIZATION ; GENETIC ENHANCEMENT ; PAIN ; RETIGABINE ; ACTIVATION ; KNOCKOUT
英文摘要

Background: Dysfunction of brain-gut interaction is thought to underlie visceral hypersensitivity which causes unexplained abdominal pain syndromes. However, the mechanism by which alteration of brain function in the brain-gut axis influences the perception of visceral pain remains largely elusive. In this study we investigated whether altered brain activity can generate visceral hyperalgesia.

Results: Using a forebrain specific alpha CaMKII promoter, we established a line of transgenic (Tg) mice expressing a dominant-negative pore mutant of the Kv7.2/KCNQ2 channel which suppresses native KCNQ/M-current and enhances forebrain neuronal excitability. Brain slice recording of hippocampal pyramidal neurons from these Tg mice confirmed the presence of hyperexcitable properties with increased firing. Behavioral evaluation of Tg mice exhibited increased sensitivity to visceral pain induced by intraperitoneal (i.p.) injection of either acetic acid or magnesium sulfate, and intracolon capsaicin stimulation, but not cutaneous sensation for thermal or inflammatory pain. Immunohistological staining showed increased c-Fos expression in the somatosensory SII cortex and insular cortex of Tg mice that were injected intraperitoneally with acetic acid. To mimic the effect of cortical hyperexcitability on visceral hyperalgesia, we injected KCNQ/M channel blocker XE991 into the lateral ventricle of wild type (WT) mice. Intracerebroventricular injection of XE991 resulted in increased writhes of WT mice induced by acetic acid, and this effect was reversed by co-injection of the channel opener retigabine.

Conclusions: Our findings provide evidence that forebrain hyperexcitability confers visceral hyperalgesia, and suppression of central hyperexcitability by activation of KCNQ/M-channel function may provide a therapeutic potential for treatment of abdominal pain syndromes.

语种英语
WOS记录号WOS:000296918300001
项目编号30630017 ; 30970919 ; 2007CB512100 ; B07001
资助机构National Science Foundation of China ; Ministry of Science Technology of China ; Ministry of Education of China
引用统计
被引频次:9[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/400002259/63435
专题北京大学基础医学院_神经生物学系
北京大学药学院_分子与细胞药理学系
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Neurobiol, Neurosci Res Inst, Beijing 100191, Peoples R China
2.Peking Univ, Dept Mol & Cellular Pharmacol, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Bi, Yeping,Chen, Hui,Su, Jun,et al. Visceral hyperalgesia induced by forebrain-specific suppression of native Kv7/KCNQ/M-current in mice[J]. MOLECULAR PAIN,2011,7(1).
APA Bi, Yeping,Chen, Hui,Su, Jun,Cao, Xu,Bian, Xiling,&Wang, KeWei.(2011).Visceral hyperalgesia induced by forebrain-specific suppression of native Kv7/KCNQ/M-current in mice.MOLECULAR PAIN,7(1).
MLA Bi, Yeping,et al."Visceral hyperalgesia induced by forebrain-specific suppression of native Kv7/KCNQ/M-current in mice".MOLECULAR PAIN 7.1(2011).
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