4  总结

　　视网膜神经节细胞的凋亡与基因表达的关系尚未起步，现认为谷氨酸释放、Ca2+内流可能使神经营养素改变，而神经营养素、NO、氧自由基可能调控谷氨酸的释放，而谷氨酸、Ca2+、NO、自由基又可作为凋亡的刺激因素，通过一系列信息传递激活凋亡基因，触发凋亡，构成恶性循环。谷氨酸及其受体抑制剂的研究有可能打破此循环，有效的保护视网膜神经节细胞。从青光眼神经细胞凋亡的机制入手，阻断其使动因素以及调控基因的控制研究，将在今后青光眼研究的深入发展中起到很大的促进作用，为青光眼的治疗展现一个广阔的前景。

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