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. 2019 Jul 10;39(28):5562–5580. doi: 10.1523/JNEUROSCI.1760-18.2019

Figure 2.

Figure 2.

Anterograde axonal transport is stalled when NgR1-dependent phosphorylation of CRMP2 is potentiated in dystrophic axons during EAE progression. A, Schematic diagram of proximal, intermediate, and distal segments (400 μm apart) of optic nerves. Representative images from right (rAAV2 transduced) and left (rAAV2 uninjected) optic nerve of (B) rAAV2-CRMP2T555A-eGFP-injected ngr1+/+ mice, (C) rAAV2-eGFP-iCre-injected ngr1flx/flx mice, and (D) rAAV2-eGFP-mNgR1-injected ngr1−/− mice. Scale bar, 70 μm. E, Number of eGFP+ rAAV2-transduced axons and accumulation of intense Alexa Fluor 555 ChTxβ in eGFP+ degenerative axons per square millimeter of sections from optic nerve, at the peak stage of EAE (n = 3, mean ± SEM, one-way ANOVA with Tukey's post test; ****p < 0.0001). F, Percentage of rAAV2-transduced axons that are dystrophic (n = 3, mean ± SEM, one-way ANOVA with Tukey's post test; *p < 0.05). G, The intensity of ChTxβ+ dystrophic axons in the area of rAAV2-transduced axons (n = 3, mean ± SEM, one-way ANOVA with Tukey's post test; **p < 0.01, ***p < 0.001). H, I, Anterograde ChTxβ transport at peak stage of EAE in (H) rAAV2-transduced right optic nerve, and (I) rAAV2 uninjected contralateral optic nerve (n = 3, mean ± SEM, one-way ANOVA with Tukey's post test; **p < 0.01, ***p < 0.001). For the net velocity of in vitro axonal transport with and without stimulation of Nogo-66 (Figure 2-1).