Fig. 7

Ablation of CXCR4 and AR in astrocytes and CXCR4 gain of function. a–c CXCR4 (a), GFAP (b) and MBP (c) immunostaining were quantified within the LPC lesion at 30 dpl of castrated male CXCR4^GFAPCre (inactivation of CXCR4 in astrocytes), CXCR4^Lox/Lox (exon 2 LoxP-flanked) and unfloxed wildtype mice. CXCR4^GFAPCre and CXCR4^Lox/Lox mice were treated during 4 weeks with a T-filled implant, whereas the wildtypes received an empty implant. d–f, CXCR4 (d), GFAP (e) and MBP (f) immunostaining were quantified within the LPC lesion at 15 dpl of castrated male CXCR4^+/1013 mice (heterozygous CXCR4 gain of function mutation) and wildtype mice receiving an empty or T filled implant. g–i CXCR4 (g), GFAP (h) and MBP (i) immunostaining were quantified within the LPC lesion at 30 dpl of castrated male wildtype mice, CXCR4^+/1013 mice and the corresponding littermate control mice. j, k, A role for astrocytic AR in the remyelinating effects of testosterone. In castrated AR^NesCre mice (inactivation of AR within the CNS), T treatment failed to stimulate remyelination within the LPC lesion (j). In transgenic AR^GFAPCre mice (inactivation of AR in astrocytes), the remyelinating action of T was also significantly reduced (k). Data are presented as means ± S.E.M. (one-way ANOVA with Tukey's multiple comparisons tests). Asterisks mark significant differences. ***P < 0.001, **P < 0.01, *P < 0.05