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Development of a-wave response in the infant eye

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Abstract

The leading edge of the electroretinogram a-wave provides information on adult rod photoreceptor function at the level of phototransduction biochemistry.1 A similar approach may be taken in the study of infant photoreceptor development. Postnatal development of the infant photocurrent component, as represented in the a-wave, will depend on maturation of photoreceptors in size, shape and transduction biochemistry. This study evaluates a-wave response to a brief (1.5 ms), white flash, full field stimulus over a large intensity range in 10 full term infants, aged 5 days to 13 months, in terms of a-wave kinetics with a model of the G-protein mediated phototransduction cascade1,2. Results are given in terms of amax, maximum a-wave amplitude at high intensity, and model parameters A, an “amplification constant” interpretable in terms of transduction biochemistry, and teff, a brief delay. In the youngest infants, araax and A were both reduced by a factor of about 4 compared to adult values, increasing rapidly over the first 100 days of life and more slowly thereafter. Photoreceptor shortening can account for the lower amax values, but it alone cannot account for lower values of A, which require altered amplification in one or more of the activation stages of transduction.

© 1993 Optical Society of America

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