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Shin Hae Park, Jun-Sub Choi, Choun-Ki Joo; Post-ischemic Glial Response in A Rodent Model of Non-Arteritic Anterior Ischemic Optic Neuropathy. Invest. Ophthalmol. Vis. Sci. 2013;54(15):1423.
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We established a rodent model of non-arteritic anterior ischemic optic neuropathy (rAION) and investigated the glial responses of the optic nerve head (ONH) following the ischemic insult of optic nerve.
Optic nerve ischemia was induced using laser-coupled Rose Bengal dye photoactivation in Sprague-Dawley rats. Optic nerve circulation was visualized by FITC-Dextran angiography. We investigated morphological changes in the ONH and retina following the induction of rAION. Post-ischemic glial responses were evaluated immunohistochemically using microglial (OX-42), astrocyte (Glial fibrillary acidic protein, GFAP) and extrinsic macrophage (F4/80) markers.
The peripapillary circulartion was markedly reduced in rAION eyes at 1 day after induction of rAION. Four weeks after rAION induction, there was a severe retinal ganglion cell (RGC) loss. TUNEL positive cells were detected only in the ganglion cell layer (GCL). Electron microscopy showed many degenerating axons with a loss of normal axon bundles and increased fibrovascular septal thickening in ONH of rAION model. The strong GFAP immunoreactivity was observed in ONH at 3 days and 1 week following rAION induction. At 2 and 4 weeks after induction of rAION, the OX-42 immunoreactivity increased. The number of F4/80-positive cells increased with a peak level at 3 days and then gradually decreased.
We established a rodent model of AION with selective RGC loss through selective insufficiency to the microcirculation around the ONH. rAION induction using laser coupled Rose Bengal dye photoactivation caused activation of glial cells and recruitment of extrinsic macrophage into the injured ONH, which might contribute to the damage of the retina and ONH following acute ischemic insults.
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