Histological evaluation of postnatal retinal development of senescence-accelerated OXYS rats

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Darya V. Telegina1, Anna K. Antonenko2, Oyuna S. Kozhevnikova3
1ICG SB RAS, Novosibirsk, Russia, telegina@bionet.nsc.ru
2NSU, Novosibirsk, Russia, antonenko-98@bk.ru
3ICG SB RAS, Novosibirsk, Russia, oidopova@bionet.nsc.ru

De novo neurogenesis in the adult mammalian retina very limited. Thereby the structural and functional features formed during the period of maturation and formation of retina can have long-term effects on the further ontogenesis of the tissue, however, the mechanisms of these disorders remain unclear. Using model of premature aging OXYS rats we investigatedВ  the early histopathological changesВ  during postnatal retinal neurogenesis. OXYS rats spontaneously develop a retinopathy similar to age-related macular degeneration (AMD). AMD is a complex neurodegenerative disease resulting in a loss of central vision in the elderly. Ganglion, horizontal, and amacrine cells are born in the embryonic phase of rat developmen. Quantitative analysis showed decreasing amacrine cells in OXYS rats as compared Wistar rats (control). At the age of P0 and P1, the number of ganglion and horizontal cells increased in OXYS rats as compared Wistar rats. Bipolar neurons, photoreceptors and MГјller glia are born postnatally. We did not find changes in Muller cells. The number of photoreceptor\’s nuclei per column in Wistar rats increased at the age of P10 and decreased at the age of P14. In OXYS rats, maximum of number of nuclei per column accounted for age of P14 and then decreased. The number of rod bipolar neurons gradually increased by age of P14 in Wistar rats and P10 in OXYS rats. Our results indicating an alteration of retinal formation in OXYS rats during the postnatal period, which may contribute to the early development of their signs of AMD.

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antoncybko@mail.ru
Anton Tsybko
3 years ago

It follows from your data that the abnormalities in the development of the retina in the OXYS rats are observed already in the early stages of postnatal development. In this respect I have two questions.
1) Do you assume that humans have similar changes in the postnatal development of the retina, which subsequently lead to AMD?
2) How your findings are consistent with known molecular and genetic AMD risk factors in humans?

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