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Fig. 10 | Acta Neuropathologica Communications

Fig. 10

From: Repetitive mild traumatic brain injury in mice triggers a slowly developing cascade of long-term and persistent behavioral deficits and pathological changes

Fig. 10

Long-term white matter pathology shown in EM. Saggital sections through corpus callosum were examined by electron microscopy at 20 w post-injury. a In sham animals, axons were tightly compact, most of which were myelinated. b In rmTBI mice axons were less compact, with dispersed degenerating axons and demyelinated axons. c The average myelin thickness was significantly reduced in the rmTBI mice. d, e Demyelinated axons (diameter > 0.3 mm with no detectable compact myelin) were identified in sham and rmTBI sections (light yellow). f The total axon density in sham and rmTBI mice were not different from each other. However, the density and percentage of demyelinated axons was significantly higher in the rmTBI samples (g, h). Asterisk denotes statistically signficant different from shams, Student t-test; p < 0.05. Representative electron micrographs of corpus callosum exhibited various abnormalities in i, decompaction (arrowhead); dystrophic axon (asterisk); demyelinated axon (light yellow) and separation of myelin from axon (arrow). Coronal sections through corpus callosum demonstrated uniform cytoskeletal structure in sham axons (j); accumulation of vesicles in degenerating axons (k, red arrows) and myelin decompaction (l, yellow arrow heads) were found after rmTBI. Scale bar = 1 μm in a, b; scale bar = 300 nm in d, e, i

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