Early postnatal development of the visual cortex in mice with retinal degeneration

This study characterizes the early postnatal development of the visual neocortex in C3H/HeNRj mice. These mice are homozygous for the Pde6brd1 mutation, which causes retinal degeneration starting from postnatal day 7 (P7). To monitor the development of the visual cortex between P3 and P28 we used eight antigens known to be expressed at different developmental stages (Nestin, tau3, β3- Tubulin, Calbindin, Doublecortin, MAP2, Parvalbumin and NeuN). Using semiquantitative analysis we traced the expression and localization of different developmental markers throughout the layers of the visual cortex. Cortical tissue sections corresponding to the first postnatal week (P3–P6) stained positively for Nestin, tau3, β3-Tubulin and Calbindin. These proteins are known to be involved in the migration of neural progenitor cells (NPCs) within the cortical plate. At the time of eye-opening (P14), Doublecortin, MAP2 and NeuN, markers for developing and maturing neurons involved in NPC differentiation are present. Between P9 and P21 Nestin and Calbindin disappear while NeuN and Parvalbumin expression increases in the course of visual neocortex development. The findings of this study provide a snapshot of the dynamic changes in cortex formation during early postnatal development. So far, it is the first investigation on the postnatal development of the mouse visual cortex. Our results indicate that in C3H/HeNRj mice retinal degeneration during these early stages may not influence the maturation of the visual cortex. Until P28 in this mouse strain, the development of the visual neocortex is in accordance with data from other mice (C57BL/6) without retinal degeneration. Whether in older individuals of the C3H/HeNRj strain the visual neocortex will show signs of functional impairment has to be shown by future work. •For the first time we investigated the postnatal development of the visual cortex in C3H/HeNRj mice•C3H/HeNRj mice do not differ substantially in immunohistochemical development of the visual cortex from non[HYPHEN]impaired mice (C57BL/6)•We do not know whether old aged C3H/HeNRj mice show morphological and physiological changes from the normal situation – we suspect deficits.•Other cortical areas and modalities might replace the missing visual input in cortex development.•Volume of the visual cortex of 119 days old C3H/HeNRj mice is smaller than in other mouse strains (Hikishima et al., 2017).