Impoverished stimulus input does not simulate the slowed visual kinetics of retinal damage.

In the rat with normal sight, the acoustic startle reflex to a sound burst is suppressed when the sound is preceded by a brief light pulse. This effect of light in the rat with retinal damage is reduced and peak suppression is seen at a greater delay. Both observations are expected consequences of the loss of visual sensitivity that should accompany photoreceptor loss. However, in an early stage of retinal damage, the peak of the suppressive effect is so delayed that at long lead times the light flash is a more effective stimulus in the rat with the damaged retina than in the normal rat. Two experiments tested the hypothesis that this crossing over of the two groups is a secondary consequence of a nonspecific loss of visual sensitivity in the visually impaired rat. If the hypothesis is correct, reductions in the intensity or duration of the light flash and the degree of dark adaptation should model the effect in normal rats. The overall amount of reflex suppression was diminished with these manipulations, but none diminished the temporal development of reflex suppression to a degree sufficient to produce the paradoxical crossover effect characteristic of retinal damage. These data indicate that decrements in the speed of visual processing are not secondary to the changes in sensitivity that accompany retinal damage, but should be viewed as a separate and independent form of visual impairment.