Skip to main content
Figure 10 | Neural Development

Figure 10

From: Multiple non-cell-autonomous defects underlie neocortical callosal dysgenesis in Nfib-deficient mice

Figure 10

Hippocampal commissure formation in Nfib null mutants. (A-D) Colour-coded anisotropy maps of E18 wildtype (A, C) and Nfib-deficient (B, D) brains. The colour code indicates the direction of axon fibre tracts (blue, dorso-ventrally projecting tracts; red, medio-laterally projecting tracts; green, rostro-caudally projecting tracts). Sections in (A, B) are mid-sagittal views. In the wildtype (A), the three major forebrain commissures were evident; the corpus callosum (CC), the hippocampal commissure (HC) and the anterior commissure (AC). In the Nfib mutant, the anterior commissure was absent, but the corpus callosum and the hippocampal commissure were evident, although much reduced in size. (C, D) Coronal views of the brains scanned in (A, B), in which tractography (yellow lines) was performed on the hippocampal fimbria. The tracts to the hippocampal commissure and the fornix (FX) could be seen at this rostro-caudal position. In the Nfib-deficient brain (D), the size of the hippocampal commissure was reduced in comparison to that of the wildtype control (C). (E-H) The brains represented in (A, B) were cut coronally and axon tracts were revealed via expression of the axonal marker GAP43. In the wildtype (E, G), the hippocampal commissure and anterior commissure were seen crossing the midline. In the Nfib mutant (F, H), a reduced hippocampal commissure was revealed by GAP43 immunohistochemistry, and the anterior commissure was absent. Panels (G, H) are higher magnifications of the boxed regions in (E, F), respectively. Scale bars: 800 μm (A, B); 500 μm (C-F); 200 μm (G, H).

Back to article page