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J. L. Goldberg, Y. Duan, W. Kong, M. Benny, B. Watson; Characterization of a Novel Photochemically Induced Ischemic Optic Neuropathy Model. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3198.
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The mechanisms that lead to neuronal death after axonal injury are poorly understood partly due to the lack of clinically relevant animal models. Here we are using a novel photochemically induced ischemic optic neuropathy (PCI-ION) model to better understand optic nerve stroke.
The left optic nerve from Sprague-Dawley (SD) adult rats was exposed to 532 nm Nd:YAG laser irradiation delivered as high-intensity pulses for 90 seconds immediately after the photosensitizing dye Erythrosin B (ErB) was injected through the femoral vein. Evans blue was used to characterize the vessel leakage and thrombus formation in the optic nerve and DiA was used to check the integrity of retinal circulation. The histological changes after PCI-ION was examined by both H&E staining and immunohistochemistry. RGC survival was quantified by counting the number of retrogradely labeled flurogold-positive cells in the flat mounted retina.
PCI-ION led to vessel leakage indicated by Evans blue distribution outside of the vessels in the nerve without interfering the circulation of retina by DiA perfusion. One week after PCI-ion at 200mw intensity, H&E staining of the optic nerve cross sections demonstrated that the optic nerve structure was disrupted and cells were aggregated at the treated area (~700µm in length, 2/3 in depth). Immunohistochemistry revealed that PCI-ION led to glial cell activation. PCI-ION led to retrograde cell death in the corresponding retinal quadrant.
We have successfully generated a rodent model of ischemic optic neuropathy. With this model, we can explore in depth the mechanisms leading to neuronal death after axonal injury, and eventually test new therapeutic strategies to enhance survival.
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