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. 2019 Aug 20;8(8):940. doi: 10.3390/cells8080940

Figure 3.

Figure 3

CK2β-ablation in skeletal muscles altered neuromuscular synapse function and affected safety factor in >6-months-old but not in 3-months-old conditional CK2β deficient mice. (A,B) Decrement of the endplate potential amplitude in wild-type and CK2β-deficient diaphragm muscles in 3-months-old mice (A) and >6-months-old mice. (C,D) Compound muscle action potential (CMAP) measurements in 3-months-old (C) and >6-months-old (D) wild-type and CK2β-deficient diaphragms under untreated conditions and in the presence of increasing concentrations (300, 500, 800, and 1,000 nM) of d-tubocurarine. The >6-months-old CK2β-deficient animals showed a significantly higher decrement of CMAP, which was already displayed at 300 nM d-tubocurarine, thus unmasking a reduced safety factor in the absence of CK2β (*** p < 0.001; ** p < 0.01; * p < 0.05; unpaired two-tailed Student’s t-test; n = 3–5 mice, each genotype). Error bars indicate s.e.m.