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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Relationship of acute axonal damage, Wallerian degeneration, and clinical disability in multiple sclerosis

Fig. 5

NPY-Y1R does not co-localize with markers of axonal transport disturbance, neurofilament dephosphorylation or myelin proteins in EAE lesions. Immunofluorescence double labeling performed on EAE lesions in WT mice revealed only rare co-localization of NPY-Y1R (red) and early axonal transport deficits indicated by APP accumulation (green) (a–c, arrow). NPY-Y1R immunoreactivity also did not co-localize with phosphorylated neurofilaments (NF) of healthy axons (SMI31, green) (d–f) or de-, resp. non-phosphorylated NF predominantly found in damaged axons (SMI32, green) (g–i), but partly with the NF high molecular weight (NF-200, green) subunit (j–l, arrows). Double IHC of NPY-Y1R (n, red) with MBP (m, green) did not reveal any co-localization (o, inset). Inset in (o) shows NPY-Y1R+ axons, in part enwrapped by myelin, at high magnification (arrows). Scale bars=(a–o) 200 μm; (inset o) 10 μm

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