責(zé)任血管外膜及面神經(jīng)跨膜蛋白在面肌痙攣發(fā)病中的作用機(jī)制研究
[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.
【學(xué)位授予單位】:上海交通大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2014
【分類號(hào)】:R745.12
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