Crowston Jonathan G, Kong Yu Xiang G, Trounce Ian A, Dang Trung M, Fahy Eamonn T, Bui Bang V, Morrison John C, Chrysostomou Vicki
Centre for Eye Research Australia, University of Melbourne, Royal Victorian Eye and Ear Hospital, East Melbourne, Victoria, Australia.
Department of Optometry and Vision Sciences, University of Melbourne, Parkville, Victoria, Australia.
Exp Eye Res. 2015 Dec;141:3-8. doi: 10.1016/j.exer.2015.03.006. Epub 2015 Mar 7.
We describe a model of acute intraocular pressure (IOP) elevation in the mouse eye that induces reversible loss of inner retinal function associated with oxidative stress, glial cell activation and minimal loss of retinal ganglion cell (RGC) number. Young healthy mouse eyes recover inner retinal function within 7-days but more persistent functional loss is seen in older mice. Manipulation of diet and exercise further modify RGC recovery demonstrating the utility of this injury model for investigating lifestyle and therapeutic interventions. We believe that systematic investigation into the characteristics and determinants of RGC recovery following an IOP challenge will shed light on processes that govern RGC vulnerability in the early stages of glaucoma.
我们描述了一种小鼠眼内急性眼压（IOP）升高的模型，该模型可诱导视网膜内层功能可逆性丧失，伴有氧化应激、胶质细胞活化以及视网膜神经节细胞（RGC）数量的轻微减少。年轻健康的小鼠眼在7天内可恢复视网膜内层功能，但在老年小鼠中会出现更持久的功能丧失。饮食和运动的调控进一步改变了RGC的恢复情况，证明了该损伤模型在研究生活方式和治疗干预方面的实用性。我们相信，对眼压挑战后RGC恢复的特征和决定因素进行系统研究，将有助于揭示青光眼早期阶段控制RGC易损性的过程。
