Fig. 5

Minocycline suppresses early microglial activation after exposure to bright white light. Representative photomicrographs show retinal sections (a–c) stained with Iba1 (green) of control, vehicle- or minocycline-treated mice 1 day after light exposure. In healthy controls, microglial cells are only located in the plexiform layers and GCL (a). Images of light-exposed vehicle-treated mice show amoeboid microglia located in the ONL, whereas retinal structures appear unaffected 1 day after light exposure (b). Compared to vehicle-treated mice, amoeboid, reactive microglia are absent in the ONL of mice treated with minocycline (c). ONL outer nuclear layer, OPL outer plexiform layer, INL inner nuclear layer, IPL inner plexiform layer, GCL ganglion cell layer. Scale bar 50 μm. Data show representative photomicrographs (control n = 6, light exposure and vehicle treatment n = 3, light exposure and minocycline treatment n = 3/group). Retinal mRNA expression of microglia and inflammation-associated genes were determined by real-time RT-PCR at 1, 2, or 4 days after light exposure (d–i). Compared to controls, the microglial-associated markers CD68, AMWAP, and TSPO were markedly increased in vehicle-treated mice peaking 1 day after light exposure. Expression levels in minocycline-treated mice were lower at every analyzed time point (d–f). CCL2 was induced in light-exposed vehicle-treated mice, which was suppressed in the minocycline-treated group (g). Minocycline treatment also significantly reduced the expression of IL6 and iNOS, which was strongly upregulated in the vehicle-treated group (h, i). Data show mean ± SEM (control n = 6, light exposure and vehicle treatment n = 3, light exposure and minocycline treatment n = 3/group, measured in triplicates) with *p < 0.05, **p < 0.01, ***p < 0.001