Figure 3: Reduced CS levels are associated with reduced scar formation in T1KO mice.

In a and b, n=7; and in c, n=5. (a,b) Fibrotic scar areas (a) and glial scar areas (b) were smaller in T1KO mice (grey) than in WT (white) or in ChABC-treated mice (ChABC; black). Data are expressed as the mean±s.e.m. These data were compared by two-way ANOVA and Bonferroni’s post hoc pairwise comparisons; *P<0.05. (c) Glial scars in T1KO mice covered a narrow area that surrounded the lesion centre; these areas were narrower than those in WT mice (2 weeks after SCI). Data are expressed as the mean±s.e.m. Scheffe’s post hoc tests at each spinal segment showed significant differences between T1KO and WT mice at −5, −1 (caudal) and 1, 5, 6 (rostral) mm away from the lesion epicentre (*P<0.05). (d) Distribution of 5HT(+) terminals after recovery from SCI in T1KO mice was different from that in ChABC-treated (ChABC) mice. Many sprouting 5HT(+) terminals had accumulated in extracellular matrix around the cells in T1KO, but not in ChABC-treated mice. Arrows indicate the regrowing 5HT(+) terminals. Scale bar, 50 μm. (e–g) PNNs after SCI were not evident in T1KO mice. Higher (e) and lower (f) magnifications of WFA-labelled PNNs in WT and in T1KO 3 weeks after SCI. PNNs were evident in WT but not in T1KO mice. The boxed areas in f are magnified in e. Scale bars, 1 mm (e,f). (g) Coronal sections of the anterior horn were taken along the axis represented by the dotted line in f and stained via WFA or with anti-aggrecan antibody (aggrecan). In T1KO mice, WFA-labelled CS concentrated in PNN was not evident but signal from aggrecan, a core CSPG protein, was evident. Scale bars, 50 μm.