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. Author manuscript; available in PMC: 2022 Aug 1.
Published in final edited form as: Exp Eye Res. 2021 May 21;209:108630. doi: 10.1016/j.exer.2021.108630

Figure 3. Analysis of Müller glial response to photoreceptor degeneration/regeneration during acute and chronic light treatments.

Figure 3.

In undamaged retinas (A and G), Glial Fibrillary Acid Protein (Gfap) immunostaining was not observed, as Müller glia remain in a non-reactive state. In the acute group (A-E), Gfap immunolabeled (green) reactive Müller glial processes among dying photoreceptors in the outer nuclear layer, as indicated by Gfap-positive puncta (arrows). These puncta increased in number through 48 hpL (C), and by 96 hpL (D), outlines of entire hypertrophied Müller glial cells were observed (arrowheads), including strong labeling of Müller glial endfeet (asterisks). At 21 dpL (E), Gfap-positive Müller glia had returned to near baseline levels, although weak staining of Müller glia endfeet was still present in places. Graphic representation of the percent-change in Gfap immunostaining from 0 hpL at each time point (F). In the chronic group (G-K) at 18 hpL (H), Gfap-positive Müller glia endfeet were observed (asterisks). This expression pattern persisted at 48 hpL (I), 96 hpL (J), and 21 dpL (K); however, the overall intensity of staining was not significantly higher than 0 hpL retina (L). In addition, hypertrophied Müller glia cell bodies were never observed in the chronic group. Graphic representation of the percent-change in Gfap immunostaining from 0 hpL at each time point (L). hpL: hours post light onset; INL: inner nuclear layer; GCL: ganglion cell layer; asterisks in F and L: significantly different from 0 hpL (p<0.05) as determined by post-hoc Tukey test from one-way ANOVA (N=5–6 retinas per time point). Scale bar=25 microns.