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Fig. 6 | Molecular Neurodegeneration

Fig. 6

From: Counteracting roles of MHCI and CD8+ T cells in the peripheral and central nervous system of ALS SOD1G93A mice

Fig. 6

MHCI and CTLs depletion accelerates the denervation of tibialis anterior but delays that of triceps brachii muscle in SOD1 mutant mice. a Analysis of muscle denervation on tibialis anterior (TA) muscle of both, G93A+/+, G93A−/− mice and corresponding NTG littermates at 123 d and 140 d. α-Bungarotoxin (BTX, red) was used to identify the postsynaptic domain, synaptic vesicle glycoprotein 2A (SV2, green) + neurofilament (2H3, green) were used to identify presynaptic terminals. Bar, 20 μm. b For each mouse group, the percentage of occupied endplates (~ 70 bungarotoxin positive endplates randomly taken) was calculated. Data are reported as mean ± SEM of four independent experiments for each genotype at 123d and from three independent experiments for each genotype at 140 d. ****P < 0.0001 (G93A+/+ vs G93A) °°P < 0.01; °°°°P < 0.001 (G93A+/+ or G93A−/− vs NTG+/+ and NTG−/−) by two-way ANOVA with Sidak’s post-analysis. c Real-time PCR for AChR-γ transcript in the TA muscles of G93A+/+, G93A−/− mice compared to the corresponding NTG littermates. Data are normalized to β-actin and expressed as the mean ± SEM fold change ratio between G93A+/+ mice, G93A−/− mice and relative controls from four independent experiments for each genotype. *P < 0.05 (G93A−/− vs G93A+/+); °°°P < 0.001 (G93A−/− vs NTG+/+; NTG−/−); § P < 0.05 (G93A+/+ vs NTG+/+ and NTG−/−). d Analysis of muscle denervation on triceps brachii (TB) muscle of G93A+/+ and G93A−/− mice compared to corresponding NTG littermates at 140 d. α-Bungarotoxin (BTX, green) was used to identify the postsynaptic domain, synaptic vesicle glycoprotein 2A (SV2, green) + neurofilament (2H3, red) were used to identify presynaptic terminals. Bar, 20 μm. For each mouse group, the percentage of occupied endplates (~ 70 bungarotoxin positive end plates randomly chosen) was calculated. e Data are reported as mean ± SEM. Four, three, three and three independent experiments were analyzed for G93A−/−, G93A+/+, NTG+/+ and NTG−/− mice, mice, respectively. ****P < 0.0001; (G93A−/− vs G93A+/+); °°°°P < 0.0001 (G93A+/+ or G93A−/− vs NTG+/+ and NTG−/−) by One-way ANOVA with Tukey’s post-analysis. f Real-time PCR for AChR-γ transcript in the TB muscles of G93A+/+, G93A−/− mice and the corresponding NTG littermates. Data are normalized to β-actin and expressed as the mean ± SEM fold change ratio between G93A+/+, G93A−/− mice and relative controls from four independent experiments for each genotype. *P < 0.05 (G93A−/− vs G93A+/+); °°P < 0.001 (G93A+/+ vs NTG+/+; NTG−/−)

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