Abstract

Chloroquine caused muscle weakness in neuromuscular preparations of both frog and cat in doses as low as those used in clinical practice. Studies of end-plate and action potentials in the muscle fibers and action potentials in single nerve fibers showed that the muscle weakness induced by chloroquine resulted from depression of the excitability of the electrically excitable membranes of the axon and muscle fiber. This led to the decrease of action potentials of the axon resulting in the reduction of transmitter output at the end plate and decreased firing index, as well as to the decrease in the amplitude of action potential of the muscle fiber itself. It was inferred that the mechanism of action of chloroquine was similar to that of local anesthetics.

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