Wang X, Tay S S W, Ng Y K
Department of Anatomy, Faculty of Medicine, National University of Singapore, MD10, 4 Medical Drive, Singapore 117597.
Histol Histopathol. 2002 Oct;17(4):1043-52. doi: 10.14670/HH-17.1043.
The present investigation was focused on the ultrastructural changes in the neurons and glial cells in the retina of rats with experimentally-induced glaucoma. An experimental glaucoma model was created by limbal-derived vein cauterization. Animals were sacrificed at 1, 3 weeks and 3 months post-operation. Retinae were dissected and processed for electron microscopy. Neuronal degeneration was observed in all the different layers of the retina at both 1 and 3 weeks post-operation. Some degenerating neurons were found in the ganglion cell layer (GCL), inner nuclear layer (INL) and outer nuclear layer (ONL). And the dying neurons presented apoptotic-like more than necrotic neurons. Many degenerating axons and axon terminals were observed between neurons in the GCL, inner plexiform layer (IPL), INL, and outer plexiform layer (OPL). Activated astrocytes and microglial cells were present in close association with degenerating neurons and axons. The Müller cells in the INL also presented longer and darker processes with more microfilaments than in normal cells. Degenerating neuronal debris, degenerating axonal profiles and electron-dense bodies were often found in the cytoplasm of macrophages. The results suggest that both microglial cells and astrocytes are activated in the process of neuronal degeneration in the retina of experimentally-induced glaucomatous rats. It is hypothesized that they may play a protective role in removing degenerating neuronal elements in the retina after the onset of glaucoma.
本研究聚焦于实验性诱导青光眼大鼠视网膜中神经元和神经胶质细胞的超微结构变化。通过烧灼角膜缘静脉创建实验性青光眼模型。在术后1周、3周和3个月处死动物。解剖视网膜并进行电子显微镜处理。术后1周和3周时，在视网膜的所有不同层均观察到神经元变性。在神经节细胞层（GCL）、内核层（INL）和外核层（ONL）发现了一些变性神经元。并且死亡的神经元呈现出更多凋亡样而非坏死样。在GCL、内网层（IPL）、INL和外网层（OPL）的神经元之间观察到许多变性轴突和轴突终末。活化的星形胶质细胞和小胶质细胞与变性神经元和轴突紧密相连。INL中的Müller细胞也呈现出比正常细胞更长、更暗且含有更多微丝的突起。在巨噬细胞的细胞质中经常发现变性的神经元碎片、变性的轴突轮廓和电子致密体。结果表明，在实验性诱导青光眼大鼠视网膜的神经元变性过程中，小胶质细胞和星形胶质细胞均被激活。据推测，它们可能在青光眼发病后在清除视网膜中变性神经元成分方面发挥保护作用。
