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. 2012 Aug 14;153(10):4830–4837. doi: 10.1210/en.2012-1601

Fig. 3.

Fig. 3.

Antiinflammatory treatment prevents chronic stress-induced increases in GFAP in the ventral hippocampus of stress-sensitive CRF2−/− mice. A and B, Brain atlas images illustrating the brain regions analyzed for ventral (A) and dorsal (B) hippocampus, adapted from the mouse atlas (26). Boxes highlight the region corresponding to image acquisition. C–H, Representative immunofluorescence images (×10 magnification) of GFAP (red) counterstained with DAPI (nuclei, blue) in CA1 (C and F), CA3 (D and G), and dentate gyrus (E and H) of the ventral hippocampus of CVS exposed WT and CRF2−/− mice. I–K, Bar graphs illustrate semiquantitative analysis of GFAP immunofluorescence. CVS increased GFAP in both the CA1 (I) and CA3 (J) subregions of the ventral hippocampus selectively in stress-sensitive CRF2−/− mice. K, No differences were observed in the dentate gyrus. L–Q, Representative immunofluorescence images of the CA1 (L, O), CA3 (M and P), and dentate gyrus (N and Q) of the dorsal hippocampus of CVS treated WT and CRF2−/− mice. There were no significant effects of genotype or treatment on GFAP levels in the CA1 (R), CA3 (S), or dentate gyrus (T) subregions of the dorsal hippocampus. Data are presented as parameter estimates of the best-fit model + observed sd of respective groups (n = 3–4). *, P < 0.05.