高眼压视网膜损伤修复研究面临的困境在于保护措施虽然可以改善视网膜节细胞的数目与功能，但受损视功能的恢复却远低于预期水平。这提示高眼压后视功能恢复还受节细胞外的其它因素的影响。我们的前期研究发现在高眼压损伤导致明显的节细胞丢失前，视网膜内传递视觉信号的神经元之间的突触发生了重塑，同时伴有视网膜大胶质细胞活化，大胶质细胞释放的促突触发生分子血小板反应素（Trombospondin2，TSP2）表达上调，大胶质细胞激活抑制剂能抑制急性高眼压后突触功能蛋白的表达上调。我们推测：急性高眼压后视网膜突触重塑的发生可能是导致视功能恢复远低于预期的重要原因，活化的大胶质细胞很可能通过释放TSP2调控这种突触重塑过程。本项目将探索大胶质细胞在急性高眼压损伤后视网膜突触重塑中的作用及机制，为完善高眼压损伤后促视功能恢复策略在干预时间和干预目标的选择上提供新的思路。

The difficulty of researches on retinal injury and repair following high intraocular pressure (HIOP) is the limited visual function recovery far lower than expected,even though the number and function of retinal ganglion cells (RGCs) have been improved much by kinds of measures. There must be other ways affecting the recovery of visual function beside RGCs’ repair. Interestingly, our previous studies found that far earlier than obvoiusly RGCs damage, the HIOP injury caused complicated synaptic plasticity of retinal neurons,which deliver visual signals to RGCs. At the same time, macroglia was activated after HIOP. And expression of Trombospondin 2 (TSP2), a kind of macroglia derived soluble molecule promoting synaptogenesis was upregulated as well. Further, Fluorocitrate, an inhibitor of macroglia activation, could suppress the upregulation of synaptophysin (a presynaptic function protein) following acute HIOP. We speculate that the retinal synaptic plasticity may be a key reason of the limited visual function recovery under kinds of repair means following HIOP. And the activated retinal macroglia may participate this synaptic plasticity via TSP2 delivery. The present study will explore the roles and mechanisms of macroglia on the synaptic plasticity in retina following HIOP. We try to provide new evidences to retinal repair strategies for better visual function recovery on intervention time points and targets after HIOP.