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Vittorio Porciatti, Tsung-Han Chou, Xu Yang, Stanislav Tomarev; Transgenic mice expressing mutated Tyr437His human myocilin have progressive loss of retinal ganglion cell electrical responsiveness. Invest. Ophthalmol. Vis. Sci. 2013;54(15):799.
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To characterize retinal ganglion cell (RGC) function in a transgenic mouse model of open-angle glaucoma by expression of mutated human myocilin (Myoc) in the trabecular meshwork (Zhou et al, IOVS, 2008).
RGC electrical responsiveness was tested with pattern electroretinogram (PERG) in 8 Myoc-mice of different ages (4, 7, 10, and 13 months) under ketamine/xylazine anesthesia. PERGs were recorded from each eye in response to horizontal gratings of 0.05 cycles/deg and 100% contrast. Intraocular pressure (IOP) was measured with a Tonolab tonometer.
In 13 month-old Myoc mice, the PERG amplitude (mean 19.7 µV, SEM 2.1) and latency (mean 109.5 ms, SEM 7.8) were significantly different (P < 0.05) from the PERG amplitude (mean 28.1 µV, SEM 1.7) and latency (mean 81.7 ms, SEM 9.9) of 4 month-old mice. In contrast, PERGs of C57BL/6J mice aged 4 and 13 months had similar amplitudes and latencies. The IOP of older Myoc mice (19.0 mm Hg, SEM 0.7) tended to be higher than that of younger Myoc mice (17.9 mm Hg, SEM 1.05)-difference not significant.
Myoc mice display age-related changes in RGC electrical responsiveness associated with modest IOP elevation. Previous studies (Zhou et al., IOVS 2008) have shown in aged Myoc mice moderate RGC loss in the peripheral retina as well as moderate axonal degeneration in the optic nerve. As IOP, PERG and structural changes are also found in the early stages of human primary open angle glaucoma, Myoc mice may represent a useful genetic model for investigating this disease.
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