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Fig. 1 | Inflammation and Regeneration

Fig. 1

From: Immune-mediated myogenesis and acetylcholine receptor clustering promote a slow disease progression in ALS mouse models

Fig. 1

Skeletal muscle denervation atrophy in fast- and slow-progressing SOD1G93A mice. A Paw grip endurance (PaGE) test for 129SvSOD1G93A mice and C57SOD1G93A mice. The data are reported as mean ± SEM for each time point (n = 10 mice per group). B Muscle mass was calculated by measure of gastrocnemius (GCM) muscles weight of 129SvSOD1G93A mice; C57SOD1G93A mice and NTG littermates at different time points of the disease (n = 4–10). Percent muscle atrophy was calculated relative to NTG mice at PS and OS. Data are reported as mean ± SEM. Significance was calculated with 2-way ANOVA with uncorrected Fisher’s LSD post-analysis (*p ≤ 0.05, ****p ≤ 0.0001). C and D Representative confocal micrographs and analysis of innervated endplates. α-Bungarotoxin (BTX, green) was used to identify the postsynaptic domain; SV2/2H3 (red) were used to identify presynaptic terminals (scale bar: 50μm). D Percentage of innervated endplates. Data are reported as mean ± SEM (~no. 100 BTX-positive endplates per animal were randomly chosen and analysed) (n = 4). Significance was calculated with 2-way ANOVA with uncorrected Fisher’s LSD post-analysis (***p ≤ 0.001, ****p ≤ 0.0001). E and F Electromyography on hindlimb muscles of C57SOD1G93A mice and 129SvSOD1G93A mice and NTG littermates at PS, OS, and SY. Denervation (E) and compound muscle action potential (cMAP) (F) through a coaxial electrode were evaluated. Data are reported as mean ± SEM. Significance was calculated with 2-way ANOVA with uncorrected Fisher’s LSD post-analysis and RM-ANOVA (*p ≤ 0.05, **p ≤ 0.01, *** ≤ 0.001)

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