Fig. 7.

The absence of IGF-1⁺astrocytes and microglia–macrophages during demyelination and remyelination in IL-1β^−/− mice. IGF-1⁺ cells appear in the corpus callosum of wild-type mice (A) but not in IL-1β-deficient mice (B) after 5 weeks of treatment. IGF-1⁺ cells remain in the corpus callosum of wild-type mice (C) undergoing remyelination but are absent in IL-1β-deficient mice (D) after 1 week of recovery after 6 weeks of cuprizone treatment.E–J, Representative sections from wild-type mice demonstrating the colocalization of IGF-1 to GFAP⁺cells and Mac-1⁺ cells within the demyelinating corpus callosum at 4 weeks. E–G, The colocalization (arrows) of IGF-1⁺ cells (green-stained cells in E) to nearly all of the GFAP⁺ astrocytes (red-stained cells in F and overlaid inG) within the lesion. H–J, The colocalization (arrows) of a few IGF-1⁺ cells (green-stainedcells in H) to Mac-1⁺microglia–macrophages (red-stained cells inI and overlaid in J) within the lesion. Scale bars: A–D, 20 μm; E–H, 10 μm.