Histopathological changes in the retina and optic nerve in imperfect albino mutant quails with a sex-linked recessive gene were studied ontogenetically. The mutant quail showed eye enlargement 3 months after hatching. The eyes exhibited hazy corneas, lens opacities and deep anterior chambers at 18 months of age. Some ganglion cells in the retina and axons in the optic disc began to degenerate 6 months after hatching. There were many deformed or fragmented ganglion cells at 12 months of age, and axonal degeneration was observed in the optic disc. The optic disc and the retina around it became excavated. At this time, hydropic degeneration was found in the ganglion nerve fibre layer and optic nerve and a small accumulation of acid mucopolysaccharide, which was sensitive to hyaluronidase, was present in the optic disc and optic nerve. The excavation was found to be fully developed around the optic disc at 18 months and most ganglion cells showed degenerative changes. During this period, the inner plexiform and inner nuclear layers showed hydropic degeneration. At 24 months the ganglion cell and ganglion nerve fibre layers had disappeared, the thickness of the inner nuclear layer was reduced and many photoreceptor cells were totally degenerated. The optic nerve was occupied by glial cells, blood vessels and cavernous spaces in which acid mucopolysaccharide accumulated. These histopathological retinal changes in the mutant quail are very similar to those reported in experimentally induced glaucoma of other animal species and to those in human glaucoma. The usefulness of this mutant quail as an animal model for the human disease is discussed.