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Figure 5


Fig. 5. C/EBPβ deficiency impairs KA induction of pro-inflammatory mediators. (A-D) C/EBPβ+/+ and C/EBPβ–/– adult mice were injected with KA and sacrificed 24 and 72 hours post-injection. Coronal sections (30 µm) were stained with antibodies against (A,B) IL1β and (C,D) COX2. Neurotrace was used to identify neurons, and anti-GFAP and tomato lectin to detect astrocytes and microglia, respectively. IL1β expression was mainly localized in the hilus (Hil) and the molecular layers (ML) surrounding the dentate gyrus, and was completely absent in the C/EBPβ–/– mice after KA injection, compared with their C/EBPβ+/+ littermates. COX2 immunoreactivity was mainly detected in the stratum radiatum (SR) and the granule cell layer of the dentate gyrus (GL). In contrast to controls, COX2 immunoreactivity was noticeably reduced in C/EBPβ–/– mice. Confocal analysis of (B) IL1β and (D) COX2 subcellular localization indicates that IL1β is expressed primarily in glial cells, whereas COX2 immunostaining is restricted to neurons. Images are representative for experiments from five animals. Scale bars, 25 µm (A,C) and 10 µm (B,D).





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