Mechanisms of neuronal-glial-vascular interactions in the retina and the application for development of anti-glaucoma drugs

本研究旨在通过玻璃体内注射NMDA诱导的大鼠视网膜变性模型，阐明视网膜中神经元-神经胶质-血管相互作用的机制。在该模型中，NMDA处理后可见神经细胞丢失、白细胞聚集、小胶质细胞活化和血管损伤。在NMDA治疗后血管损伤之前，神经细胞丢失和小胶质细胞激活。巨噬细胞移动抑制因子(MIF)和哺乳动物靶标雷帕霉素(MTOR)的抑制剂可减弱NMDA诱导的这些反应。因此，作用于这些分子的化合物可能具有纠正神经元-胶质-血管相互作用的潜力，并最终用于青光眼的治疗。

This study aimed to clarify the mechanisms of neuronal-glial-vascular interactions in the retina using a rat model of retinal degeneration induced by an intravitreal injection of NMDA. In this model, loss of neuronal cells, accumulation of leukocytes, activation of microglia, and vascular injury were observed after NMDA treatment. Neuronal cell loss and microglia activation preceded vascular injury following NMDA treatment. Inhibitors of macrophage migration inhibitory factor (MIF) and mammalian target of rapamycin (mTOR) attenuated these NMDA-induced responses. Therefore, compounds acting on these molecules may have the potential to correct the neuronal-glial-vascular interaction and ultimately be used for the treatment of glaucoma.