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. 2019 Jan 18;116(6):2328–2337. doi: 10.1073/pnas.1810932116

Fig. 1.

Fig. 1.

CMT2A Tg mice show locomotor defects and muscle denervation but no detectable motoneuronal death. (A) Evaluation of sensory function with the von Frey test at the age of 6 and 12 mo (WT: n = 11 and CMT2A Tg: n = 12). Statistical analysis: two-way repeated-measures ANOVA (group × time) with Newman–Keuls post hoc test. (B) Evaluation of motor function with rotarod test at the age of 6 and 12 mo (WT: n = 11 and CMT2A Tg: n = 12). Statistical analysis: two-way repeated-measures ANOVA (group × time, significant group effect) with Newman–Keuls post hoc test. (C) Number of motoneurons in lumbar spinal cord of 12-mo-old animals (n = 4 for both WT and CMT2A Tg). Statistical analysis: two-tailed unpaired Student’s t test. (D) Level of innervation of soleus muscle evaluated based on the colocalization of the nerve terminal marker SV2A and acetylcholine receptor marker α-bungarotoxin in 12-mo-old WT (n = 5) and CMT2A Tg (n = 7) mice. Statistical analysis: two-tailed unpaired Student’s t test. (E) Representative photomicrographs of NMJ in WT and CMT2A Tg soleus muscle, stained with anti-SV2A antibodies and α-bungarotoxin. Note the presence of unoccupied NMJ positive for α-bungarotoxin only (indicated by an asterisk) in the CMT2A Tg mice. *P < 0.05.