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C. M. Krispel, N. A. Melling, M. E. Burns; Normal Rod Photoreceptor Function in a Mouse Model of Glaucoma. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5303.
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Glaucoma is a leading cause of blindness world-wide, and although the disease is prevalent, surprisingly little is known about the cellular and molecular mechanisms underlying the resulting optic neuropathy and retinal ganglion cell death. Several studies have suggested that retinal photoreceptors are also affected in glaucomatous eyes (eg, Panda and Jonas 1992, Nork et al 2000). The purpose of this study was to investigate whether retinal photoreceptors function normally in a common mouse model of intraocular pressure (IOP) elevation glaucoma, the DBA/2J mouse.
We used suction electrodes to record light evoked responses in rod photoreceptors of DBA/2J mice. We analyzed the amplitudes and time courses of the responses and compared these to those of wild type (c57B/6) mice. Because DBA/2J mice develop elevated IOP and glaucomatous changes later in life, we examined younger adult mice (4-6 months) as well as older mice (over 8 months).
Photoreceptors of young adult DBA/2J mice showed characteristics which were indistinguishable from those wild type mice, and their light-evoked responses were of similar amplitude and time course. Photoreceptors of older DBA/2J mice often had shorter outer segments and smaller dark currents than those of age-matched c57B/l6 control mice. On average, the response kinetics of the older DBA/2J mice were not significantly different than those of wild type mice.
Our experiments show that the fundamental machinery of rod photoreceptors is intact in the DBA/2J mouse model of glaucoma. The fact that a subset of photoreceptors from older mice have smaller dark currents suggest that rod photoreceptors may undergo early degeneration in this mouse model of glaucoma.
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