Figure 3.

Ccr2−/− mice exhibit decreased NMJ reinnervation and diminished muscle function following nerve injury and repair. A, B, WT and Ccr2−/− mice have normal NMJ morphology and innervation (arrows) in naive, uninjured muscles. C, D, NMJ reinnervation, represented by colocalization of neurofilament and motor endplate staining (arrows), was significantly decreased in Ccr2−/− mice compared with WT mice at 14 d after nerve injury and repair. A significant difference in innervation remained at 21 d (images not shown), but was mitigated by 28 d (E, F). G, Bar graph summarizes the quantitative findings according to full, partial, or no NMJ innervation (none). H, Evoked CMAPs of the TA muscle were significantly lower in Ccr2−/− mice compared with WT mice at 28 d after nerve injury and repair, despite no difference in reinnervation at that time point. NF200 Ab = axons (green), BTX = α‐bungarotoxin (endplates, red), DAPI = nuclear staining (blue). Scale bar: 50 μm. Data: mean ± SD; N = 3–6 mice/genotype/time point; *p < 0.05.