Table 1.

Prolongation of EPC decay after an extended block of synaptic activity is attributable to the upregulation of fetal-type AChRs

EPC amplitude (nA)EPC integral (nA·ms)EPC decay (ms)MEPC decay (ms)n
Control73.7 ± 5.2172.1 ± 11.61.80 ± 0.051.24 ± 0.039 muscles
Activity blocked79.2 ± 7.1323.2 ± 38.0*3.18 ± 0.28*1.42 ± 0.07***6 muscles
Control pre-αA-OIVA[K15N]101.1 ± 6.4185.0 ± 13.01.40 ± 0.051.13 ± 0.058 fibers
Control post-αA-OIVA[K15N]101.5 ± 10.1186.5 ± 20.71.32 ± 0.031.08 ± 0.028 fibers
Activity blocked pre-αA-OIVA[K15N]120.3 ± 10.9445.8 ± 38.82.99 ± 0.191.59 ± 0.066 fibers
Activity blocked post-αA-OIVA[K15N]97.2 ± 8.0203.8 ± 20.9**1.62 ± 0.09**1.06 ± 0.05**6 fibers
ClC90.0 ± 5.0236.0 ± 10.42.04 ± 0.061.32 ± 0.057 muscles
ClC, activity blocked77.8 ± 3.1217.3 ± 7.22.14 ± 0.141.31 ± 0.047 muscles

  • The top two and last two rows present data from multiple experiments on the effect of block of activity on EPCs and MEPCs. In these rows, n is the number of muscles studied (in each muscle at least six muscle fibers were studied). Statistical comparisons in these cases were done using nested ANOVA

  • ↵(*p < 0.01 vs control;

  • ↵***p < 0.05 vs control). There were no statistically significant differences between ClC and ClC endplates in which nerve activity was blocked. The third through sixth rows represent data from smaller samples of control and activity blocked endplates studied before and after αA-conotoxin OIVA[K15N]. For studies of αA-conotoxin OIVA[K15N], n is the number of muscle fibers studied, and statistical comparisons were made using a paired Student’s t test before and after toxin

  • ↵(**p< 0.01 vs pre-αA-conotoxin OIVA[K15N]). ClC, ClC-1 chloride channel null mice.