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. 2021 Dec 14;37(11):110108. doi: 10.1016/j.celrep.2021.110108

Figure 1.

Figure 1

Sarm1 haploinsufficiency delays the rate of programmed axon degeneration in vivo after sciatic nerve transection

(A) Representative images of semi-thin (1 μm) transverse sections through the sciatic nerve of 2- to 3-month-old wild-type, Sarm1 haploinsufficient, or Sarm1 homozygous null littermate mice stained with Richardson’s solution and imaged using light microscopy at 100× magnification.

(B) Number of intact axons remaining in wild-type, Sarm1 haploinsufficient, or Sarm1 homozygous null mice in uncut or cut axons at the indicated number of days after transection. A two-way ANOVA was performed, followed by Dunnett post hoc analysis to determine whether there was a difference between Sarm1 haploinsufficient and Sarm1 homozygous wild-type mice at each indicated time point indicated. ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001; ns, not statistically significant; n = 3–5 per group. Each data point corresponds to quantification of an entire tibial nerve cross-section from a single mouse.

Data are presented as mean ± SEM. The scale bar represents 100 μm.