Extended Data Fig. 4: Neuronal Ahr deletion enhances regeneration in older mice but no effect of AhR inhibition post-injury.
From: AhR inhibition promotes axon regeneration via a stress–growth switch
a, b, Long-term neuronal Ahr cKO paradigm (a). Tamoxifen (100 mg/kg i.p., daily x 5) was administered 14 months before sciatic nerve crush. IF of SCG10+ axons at 3 dpi shows enhanced regeneration in cKO mice compared to controls (b). Regeneration index: two-way ANOVA with Bonferroni correction; maximal axon length distal to lesion centre: n = 5 control, n = 6 cKO; unpaired two-tailed t-test. c, Post-injury Ahr cKO paradigm. Tamoxifen (100 mg/kg i.p., daily x 3) was administered immediately after sciatic nerve crush. At 3 dpi, SCG10+ axon regeneration was comparable between cKO and control mice (n = 5 per group). Regeneration index: two-way ANOVA with Bonferroni correction; maximal axon length distal to lesion centre: unpaired two-tailed t-test. d, Post-injury AhR antagonist treatment. SR1 (25 mg/kg), BAY-2416964 (25 mg/kg), or vehicle (DMSO) were administered daily x 3 immediately after sciatic nerve crush. At 3 dpi, IF of SCG10+ axons showed no significant differences between groups. n = 6 mice (DMSO, SR1), n = 7 (BAY). One-way ANOVA with Dunnett’s correction. Data are mean ± s.e.m.
