秋水仙碱诱导的微管解聚在背根神经节慢性压迫大鼠中通过瞬时受体电位香草酸亚型4（TRPV4）介导的痛觉过敏中的作用
Role of colchicine-induced microtubule depolymerization in hyperalgesia via TRPV4 in rats with chronic compression of the dorsal root ganglion.
作者信息
Ning Liping, Wang Chuanwei, Fan Xiaohua, Ding Xinli, Wang Yonghui, Zhang Yang, Wang Jie, Yue Shouwei
出版信息
Neurol Res. 2014 Jan;36(1):70-8. doi: 10.1179/1743132813Y.0000000261. Epub 2013 Dec 6.
The aim of this study is to investigate the effect of microtubule depolymerization by colchicine on hyperalgesia mediated by transient receptor potential vanilloid 4 (TRPV4) in a neuropathic pain model of chronic compression of the dorsal root ganglion (DRG) (hereafter termed CCD) in rat. Intrathecal administration of microtubule-depolymerizing agent, colchicine, attenuated the activated effect of 4alpha-phorbol 12, 13-didecanoate (4alpha-PDD, TRPV4 specific agonist) on mechanical and thermal hyperalgesia in CCD rats. This observation is in agreement with our in vitro experiments with DRG cells that showed a significant attenuation of 4alpha-PDD-activated Ca(2+)-influx and substance P (SP) release with the colchicine treatment. We conclude that microtubule depolymerization by colchicine can regulate pain sensitivity by depressing the hyperalgesia mediated by TRPV4.
本研究旨在探讨秋水仙碱引起的微管解聚对大鼠背根神经节慢性压迫（以下简称CCD）神经病理性疼痛模型中由瞬时受体电位香草酸亚型4（TRPV4）介导的痛觉过敏的影响。鞘内注射微管解聚剂秋水仙碱可减弱4α-佛波醇12,13-十二烷酸酯（4α-PDD，TRPV4特异性激动剂）对CCD大鼠机械性和热痛觉过敏的激活作用。这一观察结果与我们对背根神经节细胞的体外实验一致，该实验表明秋水仙碱处理可显著减弱4α-PDD激活的Ca(2+)内流和P物质（SP）释放。我们得出结论，秋水仙碱引起的微管解聚可通过抑制TRPV4介导的痛觉过敏来调节疼痛敏感性。
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