Fig. 4
Neuronal IKKβ promotes the onset of CPZ demyelination and axon damage.(Ai) LFB staining of myelin (arrowheads showing maintenance of myelin at CPZ3 in nIKKβKO mice), (Ci) apoptosis inducing factor (AIF) immunostaining of apoptotic cells, and (Di) APP immunostaining of axonal spheroids in serial brain coronal paraffin sections from nIKKβKO and IKKβff control naïve (CPZ0) or CPZ-fed CPZ3 and CPZ5 mice (arrowheads showing myelin Ai reduced APP plaques Di in nIKKβKO mice at CPZ3). Scale bars: 100μΜ. (Aii) Semiquantitative scoring of demyelination (loss of LFB staining), (B) quantitative representation of CNPase immunoreactivity of myelin and OLG by densitometry, (Cii) AIF immunoreactivity by % area covered, and (Dii) numbers of APP spheroids/mm2 tissue in the corpus callosum in groups of nIKKβKO and IKKβff control mice represented in the photographs. (E) Differential expression of neuronal Snap25 relative to GusB in total mRNA isolates taken from nIKKβKO and IKKβff control brains from CPZ0 or CPZ-fed CPZ3, CPZ5, CPZ6+1 and CPZ6+4 mice. Results are means of 2 (CPZ6+1) or 3-5 mice (for all other time points) from one representative of two independent experiments. The most relevant statistically significant differences after comparisons between groups are shown by two-way ANOVA with Bonferroni’s test (Aii, Cii, and E) and by Student’s t-test (B and Dii) *p ≤ 0.05, **p ≤ 0.005, ***p ≤ 0.001