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The Electroretinogram Components in Abyssinian Cats with Hereditary Retinal Degeneration

¹From the Departments of Biomedical Engineering and ⁵Neurobiology and Physiology, Northwestern University, Evanston, Illinois; the ²Department of Biomedical Engineering and Pritzker Institute of Biomedical Science and Engineering, Illinois Institute of Technology, Chicago, Illinois; the ³Division of Ophthalmology, Evanston Northwestern Healthcare, Glenview, Illinois; and the ⁴Departments of Medicine and Surgery, College of Veterinary Medicine, and ⁶Ophthalmology, Mason Eye Institute, University of Missouri-Columbia, Columbia, Missouri.

PURPOSE. To examine phototransduction using the a-wave and other aspects of retinal function with the intraretinal b- and c-waves at different stages of an inherited photoreceptor degeneration in Abyssinian cats.

METHODS. Vitreal and intraretinal ERGs were recorded from eight dark-adapted, anesthetized Abyssinian cats. Brief bright flashes were used to elicit vitreal a- and b-waves. Longer, weaker flashes were used to elicit intraretinal b- and c-waves. Stages 1 through 4 of the disease were characterized ophthalmoscopically. Parameters of the Lamb and Pugh a-wave model (a_max, A, and t_eff) for the Abyssinian cats were compared with those for normal cats. Light microscopy was used to count photoreceptor nuclei.

RESULTS. The maximum a-wave amplitude, a_max, was significantly smaller in stage 1, and continued to decrease (stage 1: 50% of normal, stage 2: 28%, stage 3: 27%; and stage 4: unrecordable). There was a small, but not significant, decrease in the amplification constant A from 0.24 ± 0.11 s^–2 in normal cats to 0.16 ± 0.08 s^–2 in Abyssinian cats. The intraretinal b- and c-wave amplitudes decreased most dramatically during the early stage of the disease. Affected animals had fewer photoreceptors than unaffected Abyssinians or control animals. The number of photoreceptors declined most rapidly in the inferior periphery.

CONCLUSIONS. The amplitudes of all ERG components were already reduced significantly by stage 1 and progressively declined. The lack of major changes in a-wave model parameters indicates that the degeneration is probably not due to a mutation in transduction proteins. Losses of photoreceptor function were larger than losses of photoreceptor nuclei.

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