Takatsuji K, Ito H, Watanabe M, Ikushima M, Nakamura A
J Comp Pathol. 1984 Jul;94(3):387-404. doi: 10.1016/0021-9975(84)90026-4.
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.
对具有性连锁隐性基因的不完全白化突变鹌鹑的视网膜和视神经的组织病理学变化进行了个体发育研究。突变鹌鹑在孵化后3个月出现眼睛增大。18月龄时，眼睛表现为角膜模糊、晶状体混浊和前房加深。孵化后6个月，视网膜中的一些神经节细胞和视盘轴突开始退化。12月龄时有许多变形或破碎的神经节细胞，视盘中观察到轴突变性。视盘及其周围的视网膜出现凹陷。此时，在神经节神经纤维层和视神经中发现了水样变性，视盘和视神经中存在少量对透明质酸酶敏感的酸性粘多糖积聚。18月龄时，视盘周围的凹陷完全形成，大多数神经节细胞出现退行性变化。在此期间，内网状层和内核层出现水样变性。24月龄时，神经节细胞层和神经节神经纤维层消失，内核层厚度变薄，许多光感受器细胞完全退化。视神经被胶质细胞、血管和海绵状间隙占据，其中积聚了酸性粘多糖。突变鹌鹑视网膜的这些组织病理学变化与其他动物物种实验性诱导青光眼以及人类青光眼所报道的变化非常相似。讨论了这种突变鹌鹑作为人类疾病动物模型的实用性。
