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(Investigative Ophthalmology and Visual Science. 1966;5:497-507.)
© 1966 by The Association for Research in Vision and Ophthalmology, Inc.

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Rhodopsin and the Electrical Activity of the Retina in Congenital Night Blindness

R. E. CARR 1, H. RIPPS 1, I. M. SIEGEL 1, and R. A. WEALE 2

1 Department of Ophthalmology, New York University Medical Center New York, N. Y.
2 Department of Ophthalmology, New York University Medical Center New York, N. Y.; Department of Physiological Optics, Institute of Ophthalmology, Judd Street, London, W. C l.

The inability of night-blind persons to see at low levels of illumination is usually attributed to a defect involving the biosynthesis of the visual pigment, rhodopsin. Accordingly, it has been assumed that the retinal rods of the congenital nyctalope are deficient in rhodopsin or its precursors. To test this hypothesis, fundus refiectometry was performed on two subjects, each having adifferent form of congenital night blindness (dominant and recessive, respectively). In both subjects, the concentration of rhodopsin and the rate at which it regenerated after bleaching were normal. Clearly, a photochemical basis for this anomaly is untenable. However, the electrophysiological responses of these subjects showed distinct abnormalities: (a) In the case of recessive inheritance, there toas a normal light rise in the eye's standing potential, normal a-wave potentials in the ERG, but a very much reduced scotopic b-wave. (b) In the dominant form, the light rise in the standing potential was abnormal, and all ERG responses were markedly depressed. These findings implicate the neural transmission pathways as the locus of disturbance in this anomaly. In view of a normal photochemistry, analysis of the results suggests that both the a-wave of the ERG and the light rise in the standing potential originate proximal to the outer segments of the receptors




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