Fig 1: Chronic ocular hypertension and 8-OH-DPAT upregulated EAAT2 expression in the rat retina, but this effect was reversed by WAY-100635. (A) Representative western blot of EAAT2 expression in control and glaucomatous retinas 4 weeks after EVC and in glaucoma 4W + 8-OH-DPAT retinas and glaucoma 4W + WAY-100635 retinas. The expression of the 72 kDa protein was increased in the glaucomatous retinas and in the glaucoma 4W + 8-OH-DPAT group. WAY-100635 downregulated EAAT2 expression 4 weeks after glaucoma induction. (B) Densitometric analysis of EAAT2 expression in the glaucoma 4W and drug intervention groups (n = 7). EAAT2 expression was normalized to the expression in the control retinas. ANOVA, **p < 0.01 and ***p < 0.001 vs. control retina, #p < 0.05 vs. glaucoma 4W + WAY-100635. W, week; EAAT, glutamate transporter.
Fig 2: The relative expression of glial markers (Slc1a2 and Gfap) in the dorsal hippocampus 7 days after pilocarpine-induced SE. Each dot represents one animal; the bars indicate average values and error bars show standard deviations. One-way ANOVA: Slc1a2: F2,21 = 1.4, p = 0.3; Gfap: F2,20 = 21.5, p < 0.001. Asterisks indicate significant differences between groups according to Tukey’s post hoc tests: *** p < 0.001.
Fig 3: EAAT2 immunostaining. Representative examples of EAAT2 immunostaining from the dorsal hippocampus of control (CTRL) and experimental (SE) groups. Left: maximal projection of EAAT2-stained stack. Scale bar = 25 µm. Middle: Expanded part of the image boxed in the left image. The expansion shows the structural organization of EAAT2, which forms clusters. Scale bar = 5 µm. Right: detection of EAAT2 clusters. Bar graphs show relative EAAT2 cluster density and the mean cluster diameter. Data presented as mean ± SEM. Each rhombus represents a value obtained in an individual animal. t-test, ** p < 0.01.
Fig 4: Representative western blots of GFAP and EAAT2 from the dorsal hippocampus of control (CTRL) and experimental (SE) groups. Bar graphs (means ± SEM) illustrate the expression levels of GFAP and EAAT2, which were normalized to total protein. Each rhombus represents a value obtained in individual animals. Images: the upper part shows the chemiluminescent signal, and the lower part shows the Ponceau S.
Fig 5: Staining of astrocytes (GFAP, Glt-1) and Purkinje cells (Calbindin D28K) in WT and S1R-/- mouse cerebellum slices at 12 months postinjury. (A) Representative images of GFAP, Glt-1, and Calbindin D28K staining in the grey matter of the cerebellum (total magnification = 100×, scale bar = 50 µm). OD of the GFAP (B), Glt-1 (C) staining intensity in the molecular layer of the cerebellum between the WT and S1R-/- experimental groups. (D) Total cell counts of Purkinje cells in the molecular layer of the cerebellum between WT and S1R-/- experimental groups. (E) Anatomical positions of the analyzed regions in the cerebellum (red arrows). All values are presented as the means ±SEM. p values for differences between groups were calculated using the Mann–Whitney U-test, (n = 5): ** p < 0.01, *** p < 0.001 WT vs. S1R-/-, # p < 0.05 WT sham vs. WT TBI.
Supplier Page from Abcam for Anti-EAAT2 antibody [EPR19798]