Wakisaka Hiroyuki, Hato Naohito, Honda Nobumitsu, Takahashi Hirotaka, Kisaki Hisanobu, Murakami Shingo, Gyo Kiyofumi, Mominoki Katsumi, Kobayashi Naoto, Matsuda Seiji
Department of Anatomy, Ehime University School of Medicine, Ehime 791-0925, Japan.
Exp Neurol. 2002 Nov;178(1):68-79. doi: 10.1006/exnr.2002.8035.
In 1995, we developed an animal model of transient homolateral facial nerve paralysis by inoculating Herpes simplex virus type 1 (HSV-1) into the auricle of mice. This study examined the mechanism of facial nerve paralysis in this model histopathologically. Using the immunofluorescence technique with anti-HSV-1 antibody, the time course of viral spread and the site of viral replication were investigated over the entire course of the facial nerve. Furthermore, viral replication and nerve degeneration at the site of viral replication were observed by electron microscopy. On the 7th day after inoculation, facial paralysis was observed in more than 60% of mice. Immunofluorescence study revealed HSV-1 in the geniculate ganglion, the descending root, and the facial nucleus at this stage. On the 9th day, the descending root in the sections stained with osmium looked pale, because prominent demyelination had occurred in this region; electron micrographs showed many degenerated oligodendrocytes and large naked axons. In contrast, the facial nucleus neurons showed no remarkable degeneration, despite HSV-1 particles in their cytoplasm. From these findings, we concluded that facial nerve paralysis in this model is caused mainly by facial nerve demyelination in the descending root.
1995年，我们通过将1型单纯疱疹病毒（HSV-1）接种到小鼠耳廓中，建立了一种短暂性同侧面神经麻痹的动物模型。本研究从组织病理学角度研究了该模型中面神经麻痹的机制。使用抗HSV-1抗体的免疫荧光技术，在面神经的整个过程中研究了病毒传播的时间进程和病毒复制的部位。此外，通过电子显微镜观察了病毒复制部位的病毒复制和神经变性。接种后第7天，超过60%的小鼠出现面神经麻痹。免疫荧光研究显示，此时膝状神经节、下行根和面神经核中有HSV-1。第9天，用锇染色的切片中的下行根看起来苍白，因为该区域发生了明显的脱髓鞘；电子显微镜照片显示许多变性的少突胶质细胞和粗大的无髓鞘轴突。相比之下，面神经核神经元尽管其细胞质中有HSV-1颗粒，但未显示出明显的变性。从这些发现中，我们得出结论，该模型中的面神经麻痹主要是由下行根中的面神经脱髓鞘引起的。
