Fig. 1

Migration of OPC is delayed in tPA ^−/− mice during spinal cord development. a Photomicrographs from spinal cord sections show representative images (from 3–4 mice) of Olig2 immunostaining (red) and DAPI staining (blue) in the spinal cord (right ventral horn) of WT (left column) and tPA^−/− (right column) mice at E13, E15, E17 and P0. b Corresponding quantifications of Olig2⁺ oligodendrocytes (mean ± SEM, n = 3–4 per group; *p < 0.05). c Photomicrographs from tissue sections show representative images (from 3–4 mice) of Olig2 immunostaining (red) and DAPI staining (blue) in pMN domain of WT (left column) and tPA^−/− (right column) mice at E13, E15, E17 and P0. d Corresponding quantifications of Olig2⁺ oligodendrocytes (mean ± SEM, n = 3–4 per group; *p < 0.05). e Quantification of the percentage of proliferating OLs (Ki67⁺/Olig2⁺) in the spinal cord parenchyma (right ventral horn and pMN domain) (mean ± SEM, n = 3–4 per group). E: embryonic day; ec: ependymal canal; ND: not detected; OL: oligodendrocyte; P: postnatal day; pMN domain: motor neuron progenitor domain; RVH: right ventral horn; WT: wild type. tPA ^−/− : tPA Knock-out. Scale bars: 20 μm