Inhibiting BMP4/BMPRI signaling following demyelination promotes oligodendrocyte differentiation in vivo. A, Representative micrographs of immunostaining in the caudal corpus callosi of healthy control mice (control), mice subjected to 5 weeks of cuprizone treatment (Cuprizone 5w), and mice subjected to 5 weeks of cuprizone with either vehicle (Vehicle recovery) or LDN-193189 (LDN recovery) infusion for 1 week, and immunostained with OLIG2 and either PDGFRα or CC1. B, C, Analysis of OLIG2+ cell number in healthy control mice (control), mice subjected to 5 weeks of cuprizone treatment (Cuprizone 5w), and mice infused with either vehicle (Vehicle recovery) for 1 week or LDN-193189 (LDN recovery) for 1 week. As expected, the total number of OLIG2+ cells is significantly decreased after 5 weeks of cuprizone treatment compared with controls. D, Quantification of the proportion of OLIG2+/CC1+ mature oligodendrocytes showing a significant reduction at the end of cuprizone feeding. E, LDN-193189-infused mice have a significantly higher proportion of mature oligodendrocytes compared with the vehicle control group following 1 week recovery. F, Quantification of the proportion of OLIG2+/PDGFRα+ OPCs showing a significant increase at the end of cuprizone feeding. G, LDN-193189-infused mice have a significantly smaller fraction of OPCs compared with the vehicle control group following recovery (N = 4-6 animals/group). *p < 0.05, **p < 0.01, ***p < 0.001. Scale bar, 50 µm.