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. 2019 May 14;6(2):ENEURO.0399-18.2019. doi: 10.1523/ENEURO.0399-18.2019

Figure 3.

Figure 3.

Inhibiting BMP4/BMPRI signaling exerts no influence on astrocytes or microglia in vivo. A, B, 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 treatment with either vehicle (Vehicle recovery) or LDN-193189 (LDN recovery) infusion for 1 week, and immunostained with GFAP (A) or IBA-1 (B). C, Quantification of the integrated density of GFAP immunofluorescence. There is no significant change in GFAP immunofluorescence at peak demyelination (Cuprizone 5w; left) or following the infusion of LDN-193189 (LDN recovery) for 1 week compared with control groups (Control, Vehicle; right panel). D, Quantification of the integrated density of IBA-1 immunofluorescence. There is a significant increase in IBA-1 immunofluorescence in the corpus callosum at peak demyelination (Cuprizone 5w; left); however, there is no significantly different increase in IBA-1 immunofluorescence between vehicle (Vehicle recovery) or LDN-193189 (LDN recovery) infusion during 1 week of recovery after cuprizone treatment (right; N = 4-6 animals/group). ****p < 0.0001. Scale bar, 50 µm.