Fig. 4. Deficiency of C/EBPβ ameliorates KA-induced gliosis. (A,B) C/EBPβ^+/+ and C/EBPβ^–/– adult mice were injected with vehicle (V) or KA and sacrificed 24 hours and 72 hours post injection. Coronal sections (30 µm) were stained with antibodies against (A) GFAP or (B) CD11b to detect astrocytes or microglia, respectively. A significant decrease in both astrogliosis and microgliosis is observed in C/EBPβ^–/– mice. Substantial gliosis is observed in C/EBPβ^+/+ mice after KA-injection, which is prevented in C/EBPβ^–/– mice (A). Immunohistochemical detection using anti-CD11b antibodies reveals highly ramified microglia in the hippocampus of KA-treated C/EBPβ^–/– mice (B). By contrast, in C/EBPβ^+/+ mice the activated microglial cells exhibit shorter and thicker processes, and larger cell bodies. Insets show higher magnification of the images corresponding to C/EBPβ^+/+ mice. (C,D) Quantification of the number of reactive astrocytes (C) and microglial cells (D) analyzed in the hilus, stratum radiatum or molecular layer of the hippocampus. Values are the mean ± s.e. from five different animals and two independent sections per animal. ^#P0.05, ##P0.01, ^###P0.001; vehicle vs KA-injected animals. ^*P0.05, ^***P0.001; knockout vs wild-type KA-injected animals; SR, stratum radiatum; Hil, hilus; ML, molecular layer. Images representative for each group are shown. Scale bars, 25 µm.