中山醫學大學機構典藏 CSMUIR:Item 310902500/3790
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    题名: TRPV1 mediates the uterine capsaicin-induced NMDA NR2B-dependent cross-organ reflex sensitization in anesthetized rats
    作者: Hsien-Yu Peng;Hung-Ming Chang;Shin-Da Lee;Pei-Chen Huang;Gin-Den Chen;Cheng-Hung Lai;Cheng-Yuan Lai;Chun-Hsien Chiu;Kwong-Chung Tung;Tzer-Bin Lin
    贡献者: 中山醫學大學:醫學系
    关键词: spinal cord;C-fiber;pain;desensitization
    日期: 2008
    上传时间: 2011-05-20T08:45:02Z (UTC)
    ISSN: 0363-6127
    摘要: Spinal cord-mediated cross-organ sensitization between the uterus and the lower urinary tract may underlie the high concurrence of obstetrical/gynecological inflammation and chronic pelvic pain syndrome characterized by urogenital pain. However, the neural pathway and the neurotransmitters involved are still unknown. We tested the hypothesis that the excitation of capsaicin-sensitive primary afferent fibers arising from the uterus through the stimulation of transient receptor potential vanilloid 1 (TRPV1) induces cross-organ sensitization on the pelvic-urethra reflex activity. Capsaicin (1–1,000 ?M, 0.05 ml) was instilled into the uterus to induce cross-organ reflex sensitization. Activation of capsaicin-sensitive primary afferent fibers by capsaicin instillation into the uterine horn sensitized the pelvic-urethra reflex activity that was reversed by an intrauterine pretreatment with capsaizepine, a TRPV1-selective antagonist. Intrathecal injection of AP5, a glutamatergic N-methyl-D-aspartate (NMDA) antagonist, and Co-101244, an NMDA NR2B-selective antagonist, both abolished the cross-organ reflex sensitization caused by capsaicin instillation. These results demonstrated that TRPV1 plays a crucial role in contributing to the capsaicin-sensitive primary afferent fibers mediating the glutamatergic NMDA-dependent cross-organ sensitization between the uterus and the lower urinary tract when there is a tissue injury.
    URI: https://ir.csmu.edu.tw:8080/handle/310902500/3790
    http://dx.doi.org/10.1152/ajprenal.00126.2008
    關聯: Am J Physiol Renal Physiol November 1, 2008 295:F1324-F1335
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