Hirata Y, Gyo K, Yanagihara N
Department of Otolaryngology, Ehime University School of Medicine, Japan.
Acta Otolaryngol Suppl. 1995;519:93-6. doi: 10.3109/00016489509121878.
An animal model of vestibular neuritis was developed by inoculating herpes simplex virus type 1 (HSV-1) into the auricle of mice. Postural deviation was observed in 5 of 99 mice at 6 to 8 days after inoculation. Following evaluation of the vestibular function, the animals were sacrificed and the vestibular nerves examined for histopathology and immunohistochemically. All mice developed postural deviation, presented as abnormal behaviour; they could not perform various vestibular tasks, such as gait, traversing a narrow path, climbing a rope, negative geotaxis, grasping a rod, and swimming. Degeneration of Scarpa's ganglion was observed in 4 of 5 mice that developed postural deviation, while HSV-1 antigens were found in 2 of them. No such histological findings were seen in animals with normal vestibular function.
通过将1型单纯疱疹病毒（HSV-1）接种到小鼠耳廓来建立前庭神经炎动物模型。接种后6至8天，在99只小鼠中有5只出现姿势偏差。在评估前庭功能后，处死动物并对前庭神经进行组织病理学和免疫组织化学检查。所有小鼠均出现姿势偏差，表现为行为异常；它们无法执行各种前庭任务，如步态、穿越狭窄路径、攀爬绳索、负向地性、抓杆和游泳。在出现姿势偏差的5只小鼠中有4只观察到斯卡帕神经节变性，其中2只发现了HSV-1抗原。在前庭功能正常的动物中未观察到此类组织学发现。
