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Figure S1. Negative controls of antibodies to study the cellular distribution of ephrin-A3 and EphA4 in the CA1 region of hippocampus. (a) Comparing with double immunofluorescent staining of ephrin-A3 (red) and GFAP (green), non-specific IgG instead of the ephrin-A3 antibody was used and no signal was observed in (a1), and GFAP staining in (a2) was unaffected. Scale bar = 20 μm. (b) Comparing with double immunofluorescent staining of ephrin-A3 (red) and GFAP (green), nonspecific IgG instead of the GFAP antibody was used and no signal was observed in (b2), and ephrin-A3 staining in (b1) was unaffected. Scale bar = 20 μm. (c) Comparing with double immunofluorescent staining of EphA4 (red) and NeuN (green), nonspecific IgG instead of the EphA4 antibody was used and no signal was observed in (c1), and NeuN staining in (c2) was unaffected. Scale bar = 20 μm. (d) Comparing with double immunofluorescent staining of EphA4 (red) and NeuN (green), nonspecific IgG instead of the NeuN antibody was used and no signal was observed in (d2), and EphA4 staining in (d1) was unaffected. Scale bar = 20 μm.

Figure S2. Summarizing schematic of the role of astrocytic ephrin-A3 reverse signaling mediated by EphA4 receptor in controlling the abundance of glial glutamate transporters and neuronal death under ischemic conditions. EphA4-mediated ephrin-A3 reverse signaling was a crucial mechanism for astrocytes to control glial glutamate transporters and protect hippocampal neurons from glutamate excitotoxicity under ischemic conditions.

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