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Glutamate receptor-mediated retinal neuronal injury in experimental glaucoma

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Author:: No author available

Journal Title:: Acta Physiologica Sinica

Issue:: 4

DOI:: 10.13294/j.aps.2016.0030

Key Word:: 青光眼;视网膜;Müller细胞;胶质化激活;神经节细胞凋亡;glaucoma;retina;Müller cells;gliosis;retinal ganglion cell apoptosis

Abstract：青光眼是第二大致盲性眼病,为不可逆致盲的最主要原因.视网膜神经节细胞损伤和死亡是青光眼所致视功能损害的根本原因.在青光眼视神经损伤的众多病理过程中,谷氨酸受体功能的改变是导致神经节细胞凋亡的重要因素.本研究组在大鼠慢性高眼压实验性青光眼模型上,围绕这一主题开展了一系列研究.研究结果表明,一方面,高眼压导致的众多信号变化通过直接调控谷氨酸的NMDA和AMPA受体功能参与神经节细胞的凋亡过程;另一方面,高眼压导致的细胞外谷氨酸集聚激活Müller细胞上的Ⅰ型代谢型谷氨酸受体(group Ⅰ metabotropic glutamate receptors,mGluR Ⅰ),经下调细胞膜的Kir4.1钾通道引发Müller细胞的胶质化激活,进而导致神经节细胞的凋亡.结合这些结果,本文综述了有关谷氨酸受体在实验性青光眼视网膜细胞损伤中的作用及机制的若干研究进展.

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