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. 2022 Oct 13;44(4):766–779. doi: 10.1038/s41401-022-01000-7

Fig. 1. TRPV1 deficiency exacerbates motor coordinative dysfunction and demyelination.

Fig. 1

a Experimental schematic of the cuprizone (CPZ)-induced demyelinating model. b The expression of TRPV1 protein in the corpus callosum of control or CPZ-treated mice was assessed by Western blotting and normalized with β-actin expression. c The quantification of TRPV1 expression (mean ± SEM; n = 4 mice for each group; *P < 0.05 by unpaired two-tailed t-test) in b. d Body weight change of WT and TRPV1 KO mice after CPZ treatment over time (n = 8 mice for each group; statistics performed using two-way ANOVA with Tukey’s multiple comparisons test). e Motor coordinative function was assessed by rotarod test and beam walking test (mean ± SEM; n = 8 mice for each group; *P < 0.05, ***P < 0.001 by two-way ANOVA with Tukey’s multiple comparisons test). f The expression of MBP protein was assessed using Western blotting and normalized with β-actin expression. g The quantification of MBP expression (mean ± SEM; n = 4 mice for each group; *P < 0.05, **P < 0.01, ***P < 0.001 by two-way ANOVA with Sidak’s multiple comparisons test) in f. h Representative immunofluorescent images of MBP staining in the corpus callosum (scale bar = 50 μm). i Representative TEM images showing the ultrastructure of myelin/axons in the corpus callosum (scale bar = 5 μm). j Quantification of myelinated axons (mean ± SEM; n = 3 randomly selected areas from one sample of each group; *P < 0.05, ***P < 0.001 by two-way ANOVA with Tukey’s multiple comparisons test) in i.