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目的：检测脑源性神经营养因子(BDNF)干预急性高眼压后大鼠视网膜 Müller 细胞谷氨酰胺合成酶(GS) 和谷氨酸/天冬氨酸转运体(GLAST)表达的变化,探讨 BDNF 保护节细胞(RGCs)的可能机制。方法：成年大鼠分为3个 BDNF 干预组和3个溶媒对照组并进行玻璃体内注射。2 d 后将预处理动物左眼眼压升高至闪光视网膜电图 b 波消失的临界眼压且维持缺血60 min。实验动物分别存活1、3或7 d 后通过免疫组织化学检测大鼠视网膜 GS 和 GLAST 的表达变化。结果：与正常对照组比较,溶媒对照组 GS 和 GLAST 在存活1 d 和3 d 时表达上调,7d 时下降；BDNF 干预组未出现表达明显变化。结论：BDNF 可能不是通过 Müller 细胞上调 GS 和 GLAST,降低胞外 Glu 来保护 RGCs。
AIM: To investigate the changes of glutamate synthase (GS) and glutamate / aspartate transporter (GLAST) expression induced by brain-derived neurotrophic factor (BDNF) in rat retinal Müller cells after acute ocular hypertension Possible Mechanism of BDNF Protecting Ganglion Cells (RGCs). Methods: Adult rats were divided into three groups of BDNF intervention and three vehicle control groups and injected intravitreally. After 2 days, the left eye intraocular pressure of the pretreated animals was increased to the critical intraocular pressure at which the b wave of the flash electroretinogram disappeared and the ischemia was maintained for 60 min. Rats were survived 1, 3 or 7 d respectively by immunohistochemistry after retinal GS and GLAST expression changes. Results: Compared with the normal control group, GS and GLAST in the vehicle control group were up-regulated on the 1st and 3rd day of survival and decreased on the 7th day. There was no significant change in the BDNF intervention group. Conclusion: BDNF may not protect RGCs by upregulating GS and GLAST in Müller cells and decreasing extracellular Glu.