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. 2002 Apr 30;99(10):7090–7095. doi: 10.1073/pnas.092013799

Figure 4.

Figure 4

Abnormal development of the DG in mice deficient in CXCR4. (A–D) Nissl-stained coronal sections through E18.5 wild-type (A and C) or homozygote CXCR4 mutant forebrains (B and D). C and D are higher-magnification views of A and B. Gross morphology appears similar between wild-type and mutant brains in the developing neocortex (A and B) and the developing CA fields (ca1, ca3) of the hippocampal pyramidal cell layer (C and D). By contrast, the developing dg is distinct in the wild type (C) but almost undetectable in the mutant (asterisk in D). (E and F) Coronal sections processed with in situ hybridization to show expression of NeuroD. The developing dg is distinct in a wild-type mouse (E) but not in a homozygote CXCR4 mutant (asterisk in F). (G and H) Hippocampal slices prepared from an E18.5 wild-type (G) or CXCR4 mutant mouse (H) and maintained for 7 days in vitro (7DIV). Expression of Prox1 reveals a classic, V-shaped dg in the wild-type slice. By contrast, the CXCR4 mutant slice shows a small, poorly formed dg (asterisk in H).