South Australian Institute of Ophthalmology, Hanson Institute Centre for Neurological Diseases, Adelaide, Australia.
Invest Ophthalmol Vis Sci. 2010 Dec;51(12):6448-60. doi: 10.1167/iovs.10-5284. Epub 2010 Aug 4.
Glia are the main cellular CNS elements initiating defense mechanisms against destructive influences and promoting regenerative processes. The aim of the current work was to characterize the microglial response within the visual pathway in a rat model of experimental glaucoma and to correlate the microglial response with the severity of axonal degeneration.
Experimental glaucoma was induced in each right eye of adult Sprague-Dawley rats by translimbal laser photocoagulation of the trabecular meshwork. Rats were subsequently killed at various times from 3 days to 6 weeks. Tissue sections were obtained from globes, optic nerves, chiasmata, and optic tracts for immunohistochemistry and toluidine blue staining.
This model of experimental glaucoma led to a marked activation of microglia in the retina, optic nerve, and tract. Indeed, microglial activity remained elevated, even after intraocular pressure returned to basal levels. It is postulated that this process accompanies ongoing axonal degeneration. The degree of activation in the optic nerve correlated with axonal damage. Activation was characterized by increased density and morphologic changes. Both major histocompatibility complex (MHC) class I and MHC class II surface proteins were persistently upregulated in optic nerves and localized to microglial cells; however, this did not correlate with any significant T-cell infiltration. Interestingly, MHC class II expression was not detected in the retina.
The present data may have implications for the study of the pathology associated with the visual pathway in diseases such as glaucoma.
胶质细胞是中枢神经系统中主要的细胞成分，它们启动防御机制以抵抗破坏性影响，并促进再生过程。本研究的目的是在实验性青光眼大鼠模型中描述视觉通路中的小胶质细胞反应，并将小胶质细胞反应与轴突变性的严重程度相关联。
通过对小梁网进行经巩膜激光光凝，在成年 Sprague-Dawley 大鼠的每只右眼诱导实验性青光眼。随后，在 3 天至 6 周的不同时间处死大鼠。从眼球、视神经、视交叉和视束中获取组织切片，用于免疫组织化学和甲苯胺蓝染色。
这种实验性青光眼模型导致视网膜、视神经和视束中小胶质细胞的明显激活。实际上，即使眼内压恢复到基础水平，小胶质细胞的活性仍然升高。据推测，这个过程伴随着持续的轴突变性。视神经中的激活程度与轴突损伤相关。激活的特征是密度增加和形态变化。主要组织相容性复合体（MHC）I 类和 MHC II 类表面蛋白在视神经中持续上调，并定位于小胶质细胞；然而，这与任何显著的 T 细胞浸润都没有相关性。有趣的是，MHC II 类表达在视网膜中未被检测到。
这些数据可能对研究青光眼等疾病中与视觉通路相关的病理学具有重要意义。
