Excitatory mechanisms in retinal ganglion cell death in primary open angle glaucoma (POAG).

E B Dreyer, C L Grosskreutz
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Abstract

Glaucoma is a leading cause of blindness worldwide and the second leading cause of irreversible blindness in the United States. The most common form of glaucoma, primary open angle glaucoma, is characterized by a chronically elevated intraocular pressure in the absence of any demonstrable structural abnormalities in the eye. The pathologic hallmark of glaucomatous optic neuropathy is the selective death of retinal ganglion cells, generally attributed to an elevated intraocular pressure. However, the histopathology of glaucomatous injury is strikingly similar to the pattern seen with the administration of toxic levels of glutamate. We have found that glaucoma is associated with elevated levels of intraocular glutamate-to a level toxic to ganglion cells. We propose that an elevation of vitreal glutamate may be responsible, at least in part, for the loss of ganglion cells seen in open angle glaucoma.

原发性开角型青光眼视网膜神经节细胞死亡的兴奋机制。
青光眼是世界范围内致盲的主要原因之一,在美国是导致不可逆失明的第二大原因。青光眼最常见的形式是原发性开角型青光眼,其特征是在眼睛没有任何明显的结构异常的情况下,眼压长期升高。青光眼视神经病变的病理特征是视网膜神经节细胞的选择性死亡,通常归因于眼压升高。然而,青光眼损伤的组织病理学与谷氨酸毒性水平的管理惊人地相似。我们发现青光眼与眼内谷氨酸水平升高有关,升高到对神经节细胞有毒的水平。我们认为玻璃体谷氨酸的升高可能是造成开角型青光眼中神经节细胞损失的原因,至少是部分原因。
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