Figure 3. Nf1 inactivation leads to increased gliogenesis in the CC at the expense of neurogenesis in the OB.

A BrdU pulse-chase assay from P60-P90 was performed to label newly differentiated neurons and glia. (A) Low magnification view and (B) the quantification of the overall distribution of BrdU⁺ cells in P90 control and mutant brains. Arrows identify BrdU⁺ cells in the CC and arrowheads mark the abnormal increase of BrdU⁺ cells in the mutant RMS. The dashed line marks the border of the OB and the forebrain. (C) Increased Olig2⁺/BrdU⁺ cells (arrows) were observed in the mutant CC compared to controls. (D, D’) A short-term BrdU proliferation assay was performed on P60 mice. (E) 30 days after BrdU pulse, the identity of BrdU⁺ cells in the RMS was revealed by triple or double labeling of BrdU with Pax6/GFAP (a, b), Dcx/GFAP (c, d), or Olig2 (e, f). Arrows and arrowheads: BrdU double- and single-labeling cells. (F, G) The number and ratio of BrdU⁺ cells that coexpressed Pax6, GFAP or Olig2 in the control and mutant RMS was quantified. (H) Sections of the control and mutant OB were stained for BrdU, NeuN and DAPI. The number of BrdU⁺/NeuN⁺ (arrows) and BrdU⁺/NeuN^- cells per OB surface area was quantified in (H’). All the quantification data are presented as mean ± SEM. *, lateral ventricle. Scale bars: 50 μm. See also Figure S4.