AbstractIn previous electrophysiological experiments from hypopigmented animals (mice, rats, rabbits), single-unit recordings from both retinal ganglion axons and cells in the superior colliculus have demonstrated an increase in threshold in the dark-adapted state which is roughly proportional to the animal's ocular melanin concentration. We have examined the thresholds in hypopigmented mice by using a behavioral water maze screening test and found similar threshold elevations to the electrophysiology. In the present study, we investigated the contribution of retinal light damage to the threshold elevation in an albino mouse strain which is relatively resistant to light damage (C57BL/6J c2J/c2J) and mice with profound retinal degeneration (C57BL/6J rd/rd).Black or albino littermates (C57BL/6J + / c2J or c2J / c2J) were placed in either constant light (350 cd/m2) or dim cycling light (0.001 cd/m2) for 21 days before testing. The normally pigmented animals had thresholds of 1.00 × 10−5 cd/m2 regardless of their light history. The albino mice (c2J/c2J) maintained in constant light had a slight 0.30 log unit elevation compared to their controls that were maintained in dim cycling light 6.3 × 10−4 cd/m2 (similar to previously published reports).We examined the retinal morphology of representative animals in semi-thin plastic sections. We could not detect any light damage (overall morphology or cell counts in the outer-nuclear layer) in either the normally pigmented animals or the albino mice (c2J/c2J) maintained in dim cycling light. We found extensive light damage in the albino mice (c2J/c2J) maintained in constant light (virtual absence of photoreceptor outersegments) that corresponded to the slight elevation in threshold. We conclude that the elevation in threshold found in albino mice (c2J/c2J) maintained in dim cycling light is not the result of light damage. These results support our previous findings that the sensitivity defect in hypopigmented animals is proportional to the degree of ocular hypopigmentation.
