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LIU RAN, Jiazhou Xu, Wei Chen, Zhongshu Tang; Brain ischemia induced glaucoma. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3702.
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© ARVO (1962-2015); The Authors (2016-present)
1. Exploration of specific ischemic model of visual cortex(middle cerebral artery occlusion-MCAO).2. Research glaucomaous changes caused by MCAO.3. Exploration of the mechnism of primary open-angle glaucoma.
1. the right middle cerebral artery of 4-6 weeks C57 mice was ligated, then forming the specific ischemic infarct area in the visual cortex of the mice. TTC staining was used to determine whether the infarct area was formed.2. The intraocular pressure (IOP) of mice was measured at different time points after MCAO operation, and then the eyeball and brain of the mice were cut into frozen section. TUNEL assay was used to detect the apoptosis of RGC, and RPBMS+TUNEL CO-staining was used to determine whether the apoptotic cells were RGC. The number of RGC changes at different time points was observed by Brn-3a staining. The morphological changes were observed by Nissl-Eosin staining in the brain slices.3. After MCAO, FG was injected into the superior colliculus. retina wholemount was done to observe the labeling of FG at 12 hours after injection . Retinal homogenate was done at 24 hours after injection for detecting the content of FG. tail intravenous injection of Evans blue was done to detect vascular permeability after MCAO 24 hours.
1. The mouse middle cerebral artery occlusion caused the specific ischemic infarct area in the visual cortex and could continue the following experiments.2. After MCAO, glaucomatous features including a slight increase of IOP, apoptosis and loss of retinal ganglion cells (RGCs) in the eyes of mice. At the same time, different degrees of morphological changes have also appeared in the brain. The theory of glaucome induced by brain ischemia was established.3. The function of RGC axis retrograde transport was severely damaged. The decline of axonal transport function may be the mechanism of RGC death after MCAO, but the vascular system is not involved in RGC death.
1. Visual cortex ischemia led to glaucomatous damage which match the symptoms of POAG.2. The mouse middle cerebral artery occlusion led to glaucomatous features including a slight increase of IOP, apoptosis and loss of retinal ganglion cells (RGCs).3. In a mechanism study, transmission via the optic nerve slowed down, suggesting that diminish of optic nerve transmission may be the reason for RGC degeneration. Our study offers a brand new view of POAG and calls for novel approaches for glaucoma.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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