责任血管外膜及面神经跨膜蛋白在面肌痉挛发病中的作用机制研究
发布时间：2018-11-19 10:08
【摘要】：目的：面肌痉挛病因系面神经根出脑干段受周围脑血管压迫，但其具体发病机制不明。我们前期研究发现责任血管壁外膜中交感神经末梢释放的神经递质能触发异常肌反应波(abnormal muscle response,AMR)。本研究将从责任血管和面神经两方面进一步探索面肌痉挛发病机制。 方法：采用Moller面肌痉挛动物模型，根据AMR监测结果将SD大鼠分组，扫描及透射电镜分别观察责任血管-面神经接触面，免疫组化染色法检测面神经钠通道（Nav1.1、Nav1.3、Nav1.6、Nav1.7和Nav1.8）表达情况，统计分析AMR监测结果与电镜表现、钠通道表达情况间的关系。 结果：建模完成后，11/18只大鼠监测到AMR波，电镜发现AMR阳性大鼠均存在神经-血管接触面的同时破损，而AMR阴性大鼠中仅有3/7只存在神经-血管外膜的损伤(P0.05)。免疫组化部分的实验发现，13/14只AMR(+)大鼠中Nav1.8异位高表达，，而AMR(-)大鼠中均未发现Nav1.8明显变化(P0.05)。 结论：责任血管与面神经外膜均破损是面肌痉挛发病的必要条件，面神经兴奋性增高与面神经膜上Nav1.8异位表达增多有关。
[Abstract]:Objective: the etiology of hemifacial spasm is the compression of the brain stem of facial nerve root by peripheral cerebral vessels, but its pathogenesis is unclear. Our previous study found that sympathetic neurotransmitters released in the epigastric membrane of the responsible vessel trigger abnormal muscle response wave (abnormal muscle response,AMR). This study will further explore the pathogenesis of hemifacial spasm from responsible blood vessels and facial nerves. Methods: Moller hemifacial spasm animal model was used. According to the results of AMR monitoring, SD rats were divided into two groups. The responsible vascular-facial nerve interface was observed by scanning and transmission electron microscopy, and the facial sodium channel (Nav1.1,Nav1.3,) was detected by immunohistochemical staining. The expression of Nav1.6,Nav1.7 and Nav1.8, and the relationship between AMR monitoring results, electron microscopic findings and sodium channel expression were analyzed statistically. Results: after modeling, AMR waves were detected in 11 / 18 rats, and AMR positive rats were found to be damaged at the same time. Only 3 / 7 of the AMR negative rats had neurovascular adventitia damage (P0.05). The results of immunohistochemistry showed that 13 / 14 AMR () rats had high expression of Nav1.8, while no significant changes of Nav1.8 were found in AMR (-) rats (P0.05). Conclusion: the damage of the epineurium of the responsible vessels and the facial nerve is a necessary condition for the pathogenesis of hemifacial spasm. The increased excitability of the facial nerve is related to the increase of the ectopic expression of Nav1.8 on the facial nerve membrane.
【学位授予单位】：上海交通大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R745.12
本文编号：2341976
[Abstract]:Objective: the etiology of hemifacial spasm is the compression of the brain stem of facial nerve root by peripheral cerebral vessels, but its pathogenesis is unclear. Our previous study found that sympathetic neurotransmitters released in the epigastric membrane of the responsible vessel trigger abnormal muscle response wave (abnormal muscle response,AMR). This study will further explore the pathogenesis of hemifacial spasm from responsible blood vessels and facial nerves. Methods: Moller hemifacial spasm animal model was used. According to the results of AMR monitoring, SD rats were divided into two groups. The responsible vascular-facial nerve interface was observed by scanning and transmission electron microscopy, and the facial sodium channel (Nav1.1,Nav1.3,) was detected by immunohistochemical staining. The expression of Nav1.6,Nav1.7 and Nav1.8, and the relationship between AMR monitoring results, electron microscopic findings and sodium channel expression were analyzed statistically. Results: after modeling, AMR waves were detected in 11 / 18 rats, and AMR positive rats were found to be damaged at the same time. Only 3 / 7 of the AMR negative rats had neurovascular adventitia damage (P0.05). The results of immunohistochemistry showed that 13 / 14 AMR () rats had high expression of Nav1.8, while no significant changes of Nav1.8 were found in AMR (-) rats (P0.05). Conclusion: the damage of the epineurium of the responsible vessels and the facial nerve is a necessary condition for the pathogenesis of hemifacial spasm. The increased excitability of the facial nerve is related to the increase of the ectopic expression of Nav1.8 on the facial nerve membrane.
【学位授予单位】：上海交通大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R745.12
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