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. 2017 Mar 6;11:14. doi: 10.3389/fnana.2017.00014

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Copyright © 2017 Di Pierdomenico, García-Ayuso, Pinilla, Cuenca, Vidal-Sanz, Agudo-Barriuso and Villegas-Pérez.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Microglial cell increase is due to cellular division. Photomicrographs from representative retinal cross sections of P21 P23H-1 rats (left column) and P45 RCS rats (right column) immunoreacted with antibodies against PCNA (cellular division), isolectin GS-IB4 (microglia and blood vessels) Iba1 (microglia) and GFAP (astrocytes and Müller cells). Note that the retina is thinner in P23H-1 rats due to disappearance of the photoreceptor outer segments. There was no expression of PCNA in control animals (not shown). In both dystrophic strains at these ages, PCNA was expressed in some blood vessels of the outer and inner retinal plexuses (green, A–J) that were double labeled with the lectin (red, C,D) and also in some microglial cells (green, G,G',H,H') that were double labelled with anti-Iba-1 (red, G,H,G',H') specific for microglial cells. PCNA could not be detected in Müller cells labeled with anti-GFAP antibody (red, I,J). (G',H') are insets from panels (G,H), respectively. Scale bar = 100 μm.