Skip to main content
. 2013 Jun 26;33(26):10924–10933. doi: 10.1523/JNEUROSCI.0886-13.2013

Figure 4.

Figure 4.

Quantification of how ERβ, unlike ERα, in astrocytes does not protect against demyelination, axonal loss, and reactive astrogliosis. A, Myelinated NF200 axons fewer significantly reduced in WT mice with EAE, and treatment with ERα ligand prevented demyelination in WT, but not aCKO-ERα, mice. *p < 0.05 versus WT + No EAE and WT + EAE + ERα ligand (ANOVA with post hoc Bonferroni pairwise analysis). Treatment with ERβ ligand was able to reduce demyelination in WT and aCKO-ERβ mice. *p < 0.05 versus WT + No EAE, WT + EAE + ERβ ligand, aCKO + EAE + ERβ ligand (ANOVA with post hoc Bonferroni pairwise analysis). Scale bar, 15 μm. B, Numbers of NF200 axons were significantly reduced in WT mice with EAE, and treatment with ERα ligand prevented axonal loss in WT, but not aCKO-ERα, mice. *p < 0.05 versus WT + No EAE and WT + EAE + ERα ligand (ANOVA with post hoc Bonferroni pairwise analysis). Treatment with ERβ ligand was able to prevent axonal loss in WT and aCKO-ERβ mice. *p < 0.05 versus WT + No EAE, WT + EAE + ERβ ligand, aCKO + EAE + ERβ ligand (ANOVA with post hoc Bonferroni pairwise analysis). Scale bar, 40 μm. C, Reactive gliosis staining was significantly increased in WT mice with EAE, and treatment with ERα ligand prevented this increase in WT, but not aCKO-ERα, mice with EAE. *p < 0.05 versus WT + No EAE and WT + EAE + ERα ligand (ANOVA with post hoc Bonferroni pairwise analysis). Treatment with ERβ ligand was unable to prevent reactive gliosis in WT or aCKO-ERβ mice with EAE. *p < 0.05 versus WT + No EAE (ANOVA with post hoc Bonferroni pairwise analysis). Scale bar, 122 μm. n = 6 per group.