Abstract
A developmental, posthatch loss of cutaneous and ocular melanocytes in the mutant DAM (delayed amelanotic) chicken is accompanied by severe retinal degeneration. Using a food-location task, increased ocular pigment loss was associated with increased latency of response, both developmentally in young DAMS, and among adults with differing degrees of amelanosis. Analysis of optic nerve fiber composition in normals and DAMs showed a reduction in the small diameter optic axon population in severely amelanotic DAMs. With increasing severity of ocular amelanosis among animals, reduction in the density of anterogradely transported horseradish peroxidase (HRP) reaction product was seen first in retinorecipient thalamic nuclei, subsequently in the optic tectum, and ultimately in the accessory optic nucleus. An inverse relationship was also observed between the density of HRP reaction product occurring in retinal terminal fields and density of HRP label seen in the optic tracts of the same animal. No changes in either the volume or extent of central visual nuclei were apparent in partially sighted and blind DAMs.
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