Acute and chronic damaged retinas induce microglia activation and Müller glia proliferation. At 3 wpf, undamaged Tg(mpeg1:eGFP) fish retinas display few thin and ramified microglia/macrophages (arrows) and PCNA-positive cells in the ONL and INL, corresponding to rod precursors and Müller glia/NPCs, respectively (A). In contrast, 72 h after NMDA injection of Tg(mpeg1:eGFP) fish, microglia/macrophages increase in numbers and ameboid-shaped, migrate to the inner retina, and express PCNA strongly in the INL (B). Forty-eight hours after injection, control and NMDA-injured Tg(gfap:eGFP) retinas exhibit eGFP expression in Müller glia cell bodies and apical-basal extended processes (C–D”). Control retinas possess relatively few PCNA-positive Müller glia resulting from persistent neurogenesis (arrow, C–C”), while NMDA-injured retinas display increased numbers of proliferating Müller glia (arrows, D–D”). Similar to control retinas, 3 wpf control gosh sibling retinas possess some ramified microglia/macrophages and few PCNA-positive cells (E), while gosh mutant retinas have activated microglia/macrophages in the ONL (F). The control gosh sibling retinas display proliferating Müller glia and ONL cells (G–G”), as did the gosh mutant retinas (H–H”, arrows). All sections are counterstained with DAPI to visualize the three nuclear layers. Arrows in (C–D”) and (G–H”) identify PCNA and eGFP colabeled cells; yellow arrows: identify cells shown in the insets; asterisks in the insets: PCNA and eGFP colabeled cells; ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganglion cell layer.
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