摘要
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。
Objective： To investigate the protective mechanism Of brain-derived neurotrophic factor （BDNF） on retinal ganglion cells （RGCs） through detecting expression of glutamine synthesase （GS）and glutamate/aspartate transporter （GLAST） of Mueller cells in BDNF pre-treated acute hyper-intraocular pressure rat retina. Methods： Left eyes of rats were divided into 3 BDNF pre-treated groups and 3 vehicle control groups （received intravitreal injection; the right eyes served as control. The intraocular pressure of the BDNF pre-treated （2-day） eyes was increased to make b wave of flash electroretinogragh （FERG） disappear and maintained for 60 min. 1,3 and 7days later, expression of GS and GLAST of rat retina were detected using immunohistochemistry. Resulst： Compared with normal control groups, expression of GS and GLAST of vehicle control groups were increased after 1 and 3 days and decreased gradually, while that of BDNF pre-treated groups had no remarkable changes. Conclusion： It seems that BDNF＇s protection effect on RGCs is not through up-regulating GS and GLAST in Mueller cells and decreasing extracelluar Glutamate （Glu）.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2006年第1期14-17,109,共5页
Chinese Journal of Anatomy
基金
国家自然科学基金(30100098)湖南省自然科学基金(00JJY20105)
