青光眼是全球排名第一的不可逆性致盲性眼病，早期诊断、及时治疗是保障视功能不遭受或少遭受损害的最好方法。但目前缺乏敏感而客观的指标早期诊断青光眼。研究发现视网膜突触丢失是青光眼早期特征，青光眼视网膜的突触丢失可能与发育过程中突触消除具有共同的分子机制。CD3ζ是介导中枢神经系统发育过程中突触消除的重要因子，前期我们已经证实小鼠慢性高眼压模型视网膜CD3ζ表达上升，而PSD95表达减少。据此，我们推测"CD3ζ介导青光眼视网膜的突触丢失"。本课题将建立小鼠慢性高眼压模型，观察眼压升高的不同时间点CD3ζ对视网膜突触数量、形态及功能的影响，在体外实验观察CD3ζ是否直接影响神经元突触丢失，并进一步研究高眼压下CD3ζ影响视网膜突触丢失可能的信号途径。本课题的完成不仅可以为青光眼的早期诊断提供新的检测指标，而且可以为青光眼早期治疗、采取有效措施维持视网膜内部正常的结构和视觉信号传递提供新的靶点。

Glaucoma is the first leading cause of irreversible blindness worldwide. Early diagnosis and timely treatment is the best way to protect visual function.But now there is lack of sensitive and objective target for early diagnosis of glaucoma.Current research found that loss of synapses is a hallmark of earliest stages of glaucoma. An intriguing possibility emerges that a common mechanism may underlie elimination of synapses during development and disease.CD3ζ is a important factor that mediates the synapse elimination during the development of central nervous system.Up to now，we have confirmed that CD3ζ increased in the retina of the mouse model of chronic elevated intraocular pressure,but PSD95 decreased.Accordingly, we hypothesized that "CD3 ζ mediates the synapse loss in the retina of glaucoma".To confirm this hypothesis,base on the mouse model of chronic elevated intraocular pressure,we will observe how CD3ζ affects the number,morphology and function of retinal synapse. And we will also observe whether CD3 ζ directly affects neuronal synapse loss in vitro and analyze the possible signal pathways. Base on this research,we hope to find a new way for early diagnosis of glaucoma and a new target to take effective method to maintain normal retinal structure and visual signal pathway.