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Lan Zhou, Wenjie Hu, Wei Chen, Zhongshu Tang; Nerve Fiber Break and Neuronal Leakage as Primary Lesion in Acute Angle-Closure Glaucoma. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3734.
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Glaucoma is the leading cause of blindness and, unfortunately, currently irreversible. Although the elevated intraocular pressure (IOP) has been considered as the strongest risk factor and the optic nerve head (ONH) as the critical damage site, no one has detected exactly how it happens. We elucidated how elevated IOP exerted primary biomechanical damage on never fiber and retinal neurons.
Thirty mice were used for this study. IOP in the left eye was elevated to 50 mm Hg and sustained for 2hours, and the right eye was used as acontrol. To study biomechanical damage, retina was fixed during elevated IOP. Propidium iodide was injected into the vitreous of each eye to study necrosis, whole mount(n=5) and section(n=5)of retina was achieved.Antibody to GABA, glycine transport1(GLYT-1), Parvalbumin, Brn3a were used to distinguish cell type.TUNEL was performed to study apoptosis in retinal section after 6hrs of ocular hypertension(n=5). Antibody to neurofilament, synaptic vesicle 2(sv2) were used to study NF break and leakage in retinal whole mount(n=15) fixed during elevated IOP. All photographs were achieved using confocal microscopy.
Here we show that, instead of the ONH, the elevated IOP damaged the peripheral retina directly in an acute ocular hypertension mouse model. The damage started with necrosis major in amacrine cells and minor in retinal ganglion cells (RGCs) and bipolar cells, followed by apoptosis major in RGCs and minor in amacrine cells. The immediate damage includes the break of nerve fibers and the leakage of an intracellular synaptic vesicle protein SV2
This study reveals a novel mechanism for acute ocular hypertension.
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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