Fig. 10

Degeneration and regeneration are functionally normal in the absence of CCL2. Conditioning and in vivo regeneration were done as in Fig. 4. A Axon regeneration expressed as the fraction of axons relative to the crush site every 100 μm. Each point is the mean fraction ± SEM. B Mean regeneration determined by integrating regenerating axon fluorescence to find the average axon length for each nerve. Average axon lengths are plotted as mean ± SEM. For A and B, the analysis ends at 3000 μm from the crush, because that is the length of the shortest nerve segment. n = 7 nerves per injury condition per genotype, except WT Sh CL n = 8. One WT CL nerve was excluded from analysis for violating assumption 5 (see “Materials and methods”). C–E Representative images of regenerating nerves stained for SCG10. Unconditioned growth (C), representing neuron intrinsic regeneration rate, was the same in both genotypes. Conditioned growth (D, E) was also the same in Ccl2 KOs as in WT and increased compared to unconditioned controls (compare to C). The dotted line indicates the center of the crush site which was considered to be 500 μm wide, and the solid line is 3000 μm from the crush. Scale bar is 500 μm. F Myelin clearance, quantified by LFB area and plotted as mean ± SEM. WT n = 8, Ccl2 KO n = 9. G–I Representative images of myelin stained with LFB in uninjured (G) and injured (H, I) sciatic nerves. In both genotypes, myelin has almost completely degenerated and been cleared by 7 DPI. # Indicates a significant (p < 0.05) difference between the Sh CL (unconditioned) and CL (conditioned) regeneration within a genotype