Effect And Mechanism Of Glutamate Release At Hyperxia Induced Retinal Injury In Newborn Mice

Purpose:To investigate the role of glutamate in oxygen-induced newborn mice.Methods:Newborn mice were randomized into air control group, and high oxygen treatment group in a concentration of95%oxygen for five days. Retinal injury was observed with HE staining, glutamate (Glu) concentration detected by ELISA, the expression of retinal glutamate transporter (GLAST) and glutamine synthetase (GS) mRNA were detected by Reverse-transcription polymerase chain reaction(RT-PCR) analysis.Results:1. In the high oxygen treated newborn, neovascular sprout and nuclears of the vascular endothelial cells were observed to extrude out of the retinal inner limiting membrane (ILM), indicating retinal neovascularization formation. Wherease, ILM was intact in the air control group.2.ELIASA assay results showed that glutamate concentration increased significantly in the hyperoxia group than in the air control group (p<0.05). 3. RT-PCR showed that GLAST mRNA expression decreased in high oxygen treatment group, with significant differences compared with the air control group (p<0.05).4. RT-PCR showed that GS mRNA expression decreased in high oxygen treatment group, with significant differences compared with the air control group (p<0.01).Conclusions:Hyperxia can lead to the increased glutamate concentration in the retina of newborn mice. It may be associated with the decreased expression of GLAST and GS mRNA. Excitotoxicity of over-loaded glutamate may be one of the reasons for the hyperxia-induced retinal injury.