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. 2014 Dec 1;9(12):e110571. doi: 10.1371/journal.pone.0110571

Figure 10. Reduced AChE activity but not reduced embryonic AChR expression accounts for the prolongation decay of EPCs in MuSK-MG-affected muscles.

Figure 10

(A) Estimation of 90% to 10% decay rate for EPCs of TS muscles of vehicle injected Control (solid trace) and MuSK-MG-affected (dotted trace) mice. (B) EPC 90–10% decay rate for MuSK-MG-affected mice (2366 EPCs, 40 endplates, 8 mice) is significantly (P<0.0001) less than that for vehicle injected control mice (2128 EPCs, 41 endplates, 12 mice). (C) Western blot showing no expression of fetal AChR γ subunit in diaphragm muscles of 4 control (C1-C4) and 4 MuSK-MG-affected (M1-M4) mice. Quadriceps muscle of embryonic rat (ED21) served as a positive control (+ve Control). (D) Rate of thiocholine production in homogenates of hemidiaphragm muscles of vehicle-injected control (solid lines) and MuSK-MG-affected (dotted lines) mice indicates AChE activity. (E) AChE activity of MuSK-MG-affected mice (n = 7) is significantly (* denotes P<0.05) less than that of vehicle-injected control mice (n = 6).