Allen G V, Chase T
Department of Anatomy & Neurobiology, Faculty of Medicine, Dalhousie University, Nova Scotia, B3H 4H7, Halifax, Canada.
Neuroscience. 2001;102(3):603-14. doi: 10.1016/s0306-4522(00)00519-4.
A weight drop model of focal cerebellar injury was used to identify heat shock protein induction and motor function deficits in the anesthetized, adult male, Sprague-Dawley rat. All animals were trained on a beam walking test prior to surgery. Groups of animals received severe, mild or sham weight drop injury to the lateral/paravermal region of the cerebellum. The mild and sham-injured animals showed no motor deficits in the beam walking test, whereas animals with severe cerebellar injury showed significant motor deficits in the beam walking test that approached recovery of motor function 20 days after injury. Following severe injury, induction of heat shock protein of 27kDa was observed in Purkinje cells and in neurons of the deep cerebellar nuclei, as well as Bergmann glial cells, glial cells located in the granule cell layer and the underlying white matter. Following mild injury, heat shock protein of 27kDa induction was observed in Purkinje cells and glial cells, but not in neurons of the deep cerebellar nuclei. The labeled Purkinje cells were widely distributed in the ipsilateral cerebellar cortex. Many of the glial cells that were immunostained with heat shock protein of 27kDa co-localized with cells immunoreactive for glial fibrillary acidic protein. After severe injury, heat shock protein of 72kDa was localized mainly in granule cells at the site of the trauma and in the ipsilateral deep cerebellar nuclei whereas, after mild injury, light labeling was observed only in the granule cell layer. The results demonstrate that focal cerebellar injury has profound effects on motor behavior and induces different families of heat shock proteins in specific groups of neurons and glial cells in the cerebellum.
采用局灶性小脑损伤的重物下落模型，以确定麻醉状态下成年雄性Sprague-Dawley大鼠的热休克蛋白诱导情况及运动功能缺陷。所有动物在手术前均接受了走梁试验训练。将动物分组，分别对小脑外侧/旁小叶区域进行重度、轻度或假重物下落损伤。轻度损伤和假损伤的动物在走梁试验中未表现出运动缺陷，而重度小脑损伤的动物在走梁试验中表现出明显的运动缺陷，损伤后20天运动功能接近恢复。重度损伤后，在浦肯野细胞、小脑深部核团神经元以及伯格曼胶质细胞、颗粒细胞层和其下白质中的胶质细胞中均观察到27kDa热休克蛋白的诱导。轻度损伤后，在浦肯野细胞和胶质细胞中观察到27kDa热休克蛋白的诱导，但在小脑深部核团神经元中未观察到。标记的浦肯野细胞广泛分布于同侧小脑皮质。许多用27kDa热休克蛋白免疫染色的胶质细胞与胶质纤维酸性蛋白免疫反应阳性细胞共定位。重度损伤后，72kDa热休克蛋白主要定位于创伤部位的颗粒细胞和同侧小脑深部核团，而轻度损伤后，仅在颗粒细胞层观察到轻度标记。结果表明，局灶性小脑损伤对运动行为有深远影响，并在小脑特定神经元和胶质细胞群中诱导不同家族的热休克蛋白。
