NEUROMUSCULAR EXCITATION: RESPONSES OF NORMAL AND DENERVATED MAMMALIAN MUSCLE TO BIS-TRIMETHYLAMMONIUM DECANE (C10) AND TO d-TUBOCURARINE

Abstract
Bis-Trimethylammonium decane (C10) depresses the twitch tension of innervated rat muscle and causes asphyxial death unless respiration is maintained artificially. Depression occurs without change in the action potential of motor nerve or in the capacity of muscle to respond to direct stimulation. C10 reduces end-plate potential below the amplitude necessary for initiation of a propagated electrical response in muscle fibers. C10 also reduces strength of contraction of denervated muscles stimulated directly; this action is blocked by d-tubocurarine. In both innervated and denervated muscle C10 depresses demarcation potentials, i.e., it produces partial depolarization. This action is also blocked by d-tubocurarine. Fibrillation potentials of denervated muscle are obliterated by C10 and partially suppressed by d-tubocurarine. Evidence is advanced to suggest that both drugs are active at the motor end plate and also at undefined regions along the muscle fiber.

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