The postnatal development of the retina in the normal and rodless CBA mouse: A light and electron microscopic study

Abstract

The postnatal development of the retina in control (CBA/S) and rodless (CBA/Ki) mice was studied by light and electron microscopy. In the control mice, the major increase in retinal thickness occurs between birth and seven days. The inner and outer segments begin to grow into the optic ventricle between seven and ten days with their most rapid growth occurring between 12 to 15 days; by 35 days the retina appears mature. During development, the nuclear layers become thinner while the optic ventricle (layer of rods) and the plexiform layers become thicker. At birth, the mutant or rodless retina is indistinguishable from the control; however, the inner and outer segments fail to develop beyond the primitive seven-to ten-day stage. At 15 days the outer nuclear layer becomes reduced to only a few nuclei in thickness. Many degenerating elements are found in the cavity of the optic ventricle and in the outer nuclear and plexiform layers. By 35 days the mutant retina lacks photoreceptors and is reduced in thickness to less than that at birth. The pigment epithelium is heightened in regions where degeneration is incomplete but becomes highly attenuated in regions where visual cell degeneration is complete. The optic ventricle contains the villous processes of the pigment epithelium and the fringe processes of the Miiller cells. The outer limiting membrane is contiguous with remnants of the outer plexiform layer. Between the outer plexiform layer and the inner limiting membrane, the mutant retina is normal in appearance and dimension. The delayed appearance of the smooth endoplasmic reticulum of the pigment epithelium is implicated in the failure of outer segment maturation. The role of both Miiller and pigment epithelial cells in removal of the products of retinal degeneration is discussed.During a study in the Kirschbaum Memorial Laboratory concerned with feeding patterns in different strains of inbred mice, it was found that the CBA/Ki strain showed a "freely running" circadian rhythm relative to day and night differences in food intake (Liebelt and Perry, '67; Ishiki, '68). This behavior was in contrast to the nocturnal pattern of food intake seen in CBA/S mice as well as in several other strains. Electroretinographic examination of both strains revealed the absence of the "a" wave in the CBA/Ki strain mice although it was present in the CBA/S strain (Ishiki, '68). Histological studies demonstrated that the retinae of the CBA/Ki strain lacked the photoreceptor layer whereas this layer was intact in the CBA/S strain of mice. A further compari-AM. J. ANAT., 133: 179-212.son of these two strains has been described elsewhere (Staats, '67).Keeler ('27) reported on inheritance of a retinal abnormality in white mice in which the retina lacked rods and possessed one to three cell layers in the outer nuclear layer. Genetic and developmental studies indicated that this rodless condition was hereditary and resulted from a failure of the photoreceptor layer to differentiate. Later, Bruckner ('51) reported a somewhat simil...

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Role of neuronal activity and kinesin on tract tracing by manganese-enhanced MRI (MEMRI)

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