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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Retinal glial responses to optic nerve crush are attenuated in Bax-deficient mice and modulated by purinergic signaling pathways

Fig. 8

NMDA treatment triggers microglial and macroglial activation in Bax −/− mice. Wild-type and Bax −/− mice received an intraocular injection of NMDA to confirm that Bax-deficient glia were capable of mounting an activation response. Mice were evaluated for microglial and macroglial activation 7 days post-injection. a Both wild-type and Bax −/− mice exhibited a significant increase in the expression of Aif1 and Gfap relative to control eyes. The values for Aif1 expression were not statistically different between the two genotypes, although Gfap expression was significantly higher in Bax −/− mice relative to the wild-type mice (*P < 0.05). b, c Immunofluorescence also revealed a clear increase in AIF1 labeling (red) in the retinas of Bax −/− mice, with microglia appearing in the ganglion cell layer (GCL) and inner and outer plexiform layers. d, e The expression of GFAP (green label) was also confirmed in Bax −/− mice. A clear increase in labeling was seen in the GCL, as well as through the retinal layers, indicating that Bax −/− Müller glia are capable of upregulating GFAP. a Data is presented as mean ± SD. Inner nuclear layer (INL), outer nuclear layer (ONL). DAPI nuclear counterstain (blue label). Scale bar 50 μm. For each genotype, n ≥ 3

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