Cell Death and Cell Proliferation during Histogenesis in the Rat Retina after Birth

Oh, Soo Ja; Lee, Young Suk; Lee, Moon Yong; Chun, Myung Hoon

Abstract

During development of central nervous system, cell proliferation, cell migration, cell differentiation and cell death are required. It has been reported that a number of cells are dying during development in the mammalian retinae examined so far, but the pattern of cell death has not been clarified yet. In addition. little has been studied on cell proliferation after birth. This study was conducted to identify histogenesis, cell death and cell proliferation in the retinae of the developing rats by light and electron microscopic methods as well as by immunohistochemical method using anti-proliferating cell nuclear antigen [PCNA] antiserum. The results were as follows : 1. In the developing rat, from postnatal 0 through 7 days, retina consisted of ganglion cell layer, inner plexiform layer and neuroblast layer. Neuroblast layer could be subdivided into three sublaminae : sublamina a, sublamina b and sublamina p, from postnatal 3 through 7 days. 2. From postnatal 10 days, retina consisted of ganglion cell layer, inner plexiform layer, inner nuclear layer, outer plexiform layer and outer nuclear layer. 3. Cells undergoing degeneration were observed from postnatal 0 to 13 days, and patterns of cell death were apoptosis, cytoplasmic degeneration and autophagic degeneration. 4. PCNA-immunoreactivity was seen in the cells located in sublaminae b and p of the neuroblast layer at postnatal 0 and 1 days. From postnatal 3 days PCNA immunoreactivity decreased. At 7-day-old rat, PCNA-Immunoreactive cells scattered in the distal part of sublamina p of the neuroblast layer.No immunoreactivity was observed from postnatal 10 days. These results demonstrate that retinal cell proliferation ends at postnatal 7 days, and histogenesis of retina is completed at postnatal 10 days, and superfluous cells during retinal development are eliminated by apoptosis, cytoplasmic degeneration and autophagic degeneration.