Schmidt-Kastner R, Eysel U T
Department of Neurophysiology, Medical Faculty, Ruhr-Universität Bochum, Germany.
Brain Res Bull. 1994;34(5):487-91. doi: 10.1016/0361-9230(94)90022-1.
The method of photochemically induced thrombosis was used to produce severe ischemia in the rat retina. Flat mounts of the retina were prepared at 3 h, and 1, 2, 3, 4, 6, 7, and 22 days after lesioning and Nissl-stained, which facilitated the study of the topography of the ischemic lesions. The regional variability of ischemic damage and the cytological features of ischemic cell death in the ganglion cell layer were evaluated. Neuropathological analysis showed ischemic cell damage of ganglion cells at 3 h, an infarction-type lesion at 1 to 7 days, and scar formation at 3 weeks. As an additional parameter of ischemic ganglion cell death, the degeneration of retinal axons was visualized in the contralateral dorsal lateral geniculate nucleus by Fink-Heimer silver impregnation and by immunohistochemical staining for glial fibrillary acidic protein (GFAP) in reactive astrocytes.
采用光化学诱导血栓形成法在大鼠视网膜中制造严重缺血。在损伤后3小时以及1、2、3、4、6、7和22天制备视网膜平铺片,并进行尼氏染色,这有助于研究缺血性病变的地形图。评估了神经节细胞层缺血性损伤的区域变异性和缺血性细胞死亡的细胞学特征。神经病理学分析显示,在3小时时神经节细胞出现缺血性细胞损伤,在1至7天时出现梗死型病变,在3周时出现瘢痕形成。作为缺血性神经节细胞死亡的另一个参数,通过Fink-Heimer银浸染法以及对反应性星形胶质细胞中的胶质纤维酸性蛋白(GFAP)进行免疫组化染色,在对侧背外侧膝状核中观察到视网膜轴突的变性。