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N Goldenberg-Cohen, F Margolis, NR Miller, SL Bernstein; Functional Changes in a Mouse Model of Anterior Ischemic Optic Neuropathy . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3677.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: We previously reported on the development of the first model of anterior ischemic optic neuropathy (AION) in rats (IOVS, 42;5019,2001). We now report the first description of AION in mice, and the functional changes that occur in mouse retinal ganglion cells directly resulting from AION. Methods: All animal protocols were performed using approved ARVO guidelines, and approved by IACUC. AION was induced on ketamine/xylazine anesthetized animals using a photoinducible dye and a fundus contact lens. One eye was left untreated as an internal control. We used a transgenic C57Bl6 mouse strain previously constructed with an insertion of the cFos promotor linked to the LacZ protein. Nontransgenic C57Bl6 mice were used as a control strain. Following AION induction, the animals were sacrificed at 12 hours and 1,3 and 30 days. Eyes were fixed in 2% paraformaldehyde/PBS and beta-galactosidase activity was assayed using X-Gal, which yields an insoluble blue reaction product. LacZ expression was evaluated in the lens, cornea, and retina of transgenic animals. RGC counts were performed 30 days following AION induction. Results: LacZ expression was noted at the equatorial region of the lens in the treated eye. Expression of LacZ in the retinal ganglion cell layer is also seen after treatment, following AION induction. Significant retinal ganglion cell loss was seen in the treated eye one month following AION, but not in the control eye. Conclusion: AION specifically affects RGCs. The ischemic axonopathy produced by AION directly induces RGC cellular stress. cFos expression likely plays a major role in the response of RGCs to this cellular stress, and can be directly measured by LacZ induction soon after disease onset. AION in mice produces cellular stress.
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