Abstract
The repetitive firing in curarized frog sartorius muscle caused by aconitine was found to be associated with a dose-dependent membrane depolarization and a decrease in membrane resistance (R m). Shortly after aconitine treatment, when repetitive discharges began to occur spontaneously in a few fibers (the pre-burst state), the muscle fibers were hypersensitive to mechanical and electrical stimulation. After a repetitive discharge (the post-burst state), the membrane potential fell to the 40–50 mV range. Cable measurements demonstrated that R m decreased by 27% in the pre-burst state and by 47% in the post-burst state. Substitution of choline for sodium in the post-burst state restored the membrane potential to normal and raised the R m toward the control level. It is proposed that aconitine's production of repetitive discharges in skeletal muscle is partly the result of maintaining the sodium conductance g Na at a higher-than-normal level once excitation has been initiated.
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