FKN enhances remyelination
(A) Ten-week-old C57BL/6J mice were fed cuprizone chow for 6 weeks. VC/FKN was infused into the lateral ventricle for 3 days after cuprizone cessation, and mice were returned to normal chow.
(B) Representative TEM images of CC sections from VC- and FKN-infused mice. Arrowheads designate well-preserved mitochondria, asterisks abnormal myelin, yellow and blue small and medium diameter axons, respectively, and purple glial fibrillar protein positive regions.
(C–F) Analysis of (B) for g-ratio versus axon diameter correlation (C), average g-ratio for all axons (D), and average g-ratio (E) or g-ratio frequency distribution (F) for binned axons.
(G–J) Analysis of (B) for total (G and H) or binned (I and J) myelinated axon density (G and I) or proportion (H and J).
(K) Morphometric analysis of abnormal myelin. AU = arbitrary units.
(L) Ten-week-old PDGFRαCreERT2;RosamT/mG were fed cuprizone chow for 6 weeks. Tamoxifen was injected in the last week of cuprizone treatment. VC/FKN was infused into the lateral ventricle after cuprizone cessation for 7–21 days and mice were returned to normal chow.
(M and N) Representative images of VC- (top) and FKN- (bottom) infused cortical GM immunostained for MBP (magenta) and GFP (green) after 7 (M) and 21 (N) days of infusion. White represents MBP and GFP co-localization.
(O and P) Quantification of (M), (N) normalized to VC after 7 (O) and 21 (P) days of infusion. Scale bars, 1 μm in (B), 50 μm in (M and N). Error bars represent SEM. Each data point in (C) represents an axon, and in (D–K) a mouse. Data were analyzed using unpaired t test, except data in (C and F) were analyzed with linear regression and data in (E, I, and J) with multiple t test. ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05, ns = not significant, n = 3–4 mice per group.
See also Figure S5.