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Rod Photoreceptor Dysfunction in Diabetes: Activation, Deactivation, and Dark Adaptation

¹From the Department of Optometry and Vision Sciences, University of Melbourne, Carlton, Australia; and the ²Department of Anatomy and Cell Biology, University of Melbourne, Parkville, Australia.

PURPOSE. To examine photoreceptor function in diabetes in detail by evaluating photoreceptor light activation, deactivation of the photoresponse, and recovery of the photoreceptor after bleaching (dark adaptation) in rats made diabetic with streptozotocin (STZ).

METHODS. Animals were assigned to treated and control groups. Light activation in rod photoreceptors was established using a paired-flash electroretinogram (ERG) protocol, and the leading edge of the a-wave was modeled with the mechanisms mediating phototransduction. Deactivation of the photoreceptor response was evaluated at three luminous exposures (1.4–2.2 log cd · m/s^–2) using a variable interstimulus interval (ISI) paradigm. Dark adaptation was evaluated at 90-second intervals for 30 minutes after approximately 20% pigment bleach. At each time point, a paired-flash signal (1.4 log cd · s/m^–2) was used to extract rod responses.

RESULTS. Diabetic animals showed decreased amplitudes of the photoreceptor response 12 weeks after diabetes induction. No difference was found in the rate of deactivation of the photoresponse in diabetic rats. Normalized amplitudes showed that diabetic animals had significantly faster dark adaptation (P < 0.01) than did controls.

CONCLUSIONS. Although photoreceptor activation was abnormal, deactivation was unaltered after 12 weeks of diabetes. The faster relative recovery found in diabetes after bleach, in the presence of normal pigment dynamics, may reflect a decrease in outer segment lengths.

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