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Figure 9 | Neural Development

Figure 9

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

Figure 9

Slit2 expression at the cortical midline. (A) In the wildtype at E18, expression of the axon guidance cue Slit2 was observed within the glial wedge region (arrows in (A)). (B) In the Nfib null mutant at rostral levels, expression of Slit2 was diminished (arrowhead). (C) At more caudal levels in the mutant, expression of Slit2 in the glial wedge region was more noticeable (arrows). (D) Expression of GFAP in the wildtype at E18. (E) In Nfib knockout sections at rostral levels, GFAP was observed in the glial wedge (arrows). (F) Further caudally, GFAP was observed in both the glial wedge (arrows) and indusium griseum glia (open arrowhead). (G-L) Co-immunofluorescent labelling of Nfib knockout sections at rostral (G-I) and caudal (J-L) levels with the axonal marker GAP43 (green) and the astrocytic marker GFAP (red). At rostral levels, no callosal axons could be seen crossing the midline, and few GFAP-positive glia were observed within the glial wedge (arrowheads in (H, I)). At caudal levels, however, more GFAP-positive glia were detected within the glial wedge (arrowheads in (K, L)) and GFAP-positive glia were also seen within the indusium griseum (double arrowheads in (K, L)). Callosal axons are also seen crossing the midline at this level (arrows in (J, L)). Scale bar: 200 μm.

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