视网膜小胶质细胞的内稳态（主要表现为数量的稳定）对维持视网膜的正常功能有重要意义，但其调控因素和机制尚未明确。为此，在前期研究中我们建立了研究视网膜小胶质细胞内稳态的动物模型（利用PLX5622药物清除绝大部分小胶质细胞，再停药让其数量恢复）。我们证明该模型中小胶质细胞内稳态的恢复主要源自其内源性再生；并发现和常规亮/暗交替环境相比，在暗室里小胶质细胞的内源性再生明显加速，但机制不详。我们猜想视觉刺激可能会通过谷氨酸钠-ATP途径来调控视网膜小胶质细胞的内稳态。本研究利用上述模型进一步明确哪些视觉刺激（“暗”环境、“亮”环境、闪光刺激）可以调控小胶质细胞的内源性再生，并在眼球内注射谷氨酸钠受体和ATP受体的拮抗剂来明确视觉刺激是否通过谷氨酸钠-ATP途径来调控其内源性再生。本研究提出了新的调控视网膜小胶质细胞内稳态的因素（视觉刺激），并探讨其机制，为无创加速其内稳态的恢复打下基础。

Retinal microglial homeostasis (a stable state of microglial population) is necessary for the integrity of retinal functions. However, the factors and molecular mechanisms to regulate microglial homeostasis are not well understood. So we set up an animal model to study the microglial homeostasis by using a small molecule named PLX5622 to deplete most of the retinal microglia, and then ceasing the administration of the drug to allow microglial repopulation. We confirmed that most of the repopulating microglia were originated from the endogenous regeneration of residual microglia; and found that compared with the mice under regular 12h light-12h dark condition, the mice under 24h dark condition had significantly faster microglial repopulation; however the mechanism is not known yet. We hypothesized that the visual stimulus may take part in regulating microglial homeostasis via glutamate-ATP pathway. To verify this hypothesis, Our current study is firstly to confirm that a variety of visual stimuli (dark, light, flickering light) can modulate retinal microglial repopulation based on the animal model aforementioned. And then we plan to inject intraocularly the blocker of glutamate or ATP receptor during microglial repopulation under different visual stimuli to explore whether the effect of visual stimulus on microglial repopulation was regulated via glutamate-ATP pathway. Our study can potentially find a novel factor (visual stimulus) to regulate microglial homeostasis, and by exploring the underlying molecular mechanism, we can achieve microglial homeostasis in an accelerated and non-invasive way.