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Fig. 8. Absence of significant neuronal deficit in the Olig2-ablated cortex. (A-D) The cortices from control (Ctrl^G) and Olig2-ablated (Cko^G) mice at P14 were immunostained with antibodies to NeuN (red), calbindin (red) and GABA (green), as indicated. (E,F) Gfap expression was examined by in situ hybridization in the forebrain of control Olig2C/+;Syn1^Cre (Ctrl^S) and Olig2Cko;Syn1^Cre (Cko^S) mice. (G-J) Immunostaining of Olig2 (green) and axonal proteins NF200 (red) and Tau-1 (red) in the cortex of control (Ctrl^G; G,I) and Olig2 mutant (Cko^G; H,J) mice. (K-N) Immunostaining of axonal proteins NF200 and Tau-1 in the corpus callosum (CC) of wild-type (K,M), and Olig2 mutant (Cko^G; L,N) mice. The more intense staining in the Cko^G mice, as compared with the wild-type mice, might be due to the fact that dysmyelinating axons in the Olig2 mutant are more accessible to the antibodies.

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