Grosche J, Härtig W, Reichenbach A
Carl Ludwig Institute of Physiology, Leipzig University, Germany.
Neurosci Lett. 1995 Feb 9;185(2):119-22. doi: 10.1016/0304-3940(94)11239-f.
In retinal light damage, degeneration of photoreceptors may cause alterations of glial (Müller) cells. We performed immunocytochemical studies on Müller cells isolated from retinae of rats exposed to enhanced illumination for 24 months, a procedure which leads to complete loss of photoreceptor cells. One group of rats was fed daily with Ginkgo biloba extract (EGb 761, an established free radical-scavenger) during the last 8 months of life when the remaining photoreceptors (about 50%) die. We found that (1) Müller cells respond to photoreceptor damage by increased expression of glial fibrillary acidic protein, (2) Müller cells reduce expression of glutamine synthetase when the major glutamate-releasing neurons are lost, and (3) the application of exogenous free radical scavengers prevents the expression by Müller cells of the protooncogene protein Bcl-2, a molecule assumed to activate endogenous free radical-scavenging activities.
在视网膜光损伤中，光感受器的退化可能导致神经胶质（穆勒）细胞的改变。我们对从暴露于强光24个月的大鼠视网膜中分离出的穆勒细胞进行了免疫细胞化学研究，该过程会导致光感受器细胞完全丧失。一组大鼠在生命的最后8个月每天喂食银杏叶提取物（EGb 761，一种已证实的自由基清除剂），此时剩余的光感受器（约50%）死亡。我们发现：（1）穆勒细胞通过增加胶质纤维酸性蛋白的表达来应对光感受器损伤；（2）当主要的谷氨酸释放神经元丧失时，穆勒细胞会降低谷氨酰胺合成酶的表达；（3）应用外源性自由基清除剂可阻止穆勒细胞表达原癌基因蛋白Bcl-2，该分子被认为可激活内源性自由基清除活性。
