The Neuromuscular Blocking Action of an Isolated Toxin from the Elapid (Oxyuranus scutellactus)

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Abstract
Intravenous administration of the neurotoxin (taipoxin) to mice caused after a latent period death by respiratory paralysis. The length of the latent period varied with dose, the dose‐response relation being bilogarithmic. Taipoxin failed to affect the resting membrane potential and the action potential of muscle. It caused a slight reduction in the acetylcholine sensitivity of the muscle membrane. The main effect of taipoxin on neuromuscular transmission was to reduce spontaneous and evoked transmitter release. The frequency of spontaneous miniature end‐plate potentials (m.e.p.p.s) was reduced to complete stop and depolarization of nerve terminals by a high potassium concentration (20 mM) failed to cause a marked and sustained increase in m.e.p.p. frequency. With nerve stimulation the amplitude of end‐plate potentials (e.p.p.s.) was reduced and with repetitive stimulation the amplitude of e.p.p.s. rapidly fell to a low level. Post‐tetanic facilitation of m.e.p.p. frequency and of e.p.p. amplitude were absent. The shape of evoked e.p.p.s. indicated asynchronous release of transmitter quanta. The effects of the toxin on neuromuscular transmission progressed even when the muscle was removed from the animal and placed in toxin‐free bathing fluid. In vitro experiments showed that the rate of onset of neuromuscular block depended on the temperature of the bathing solution and on the degree of activity at the neuromuscular junction. Thus, incubation in toxin solution during 4 hr at 28° C failed to produce a neuromuscular block while at 37° C the block was complete within 1 h. With nerve stimulation at 10 Hz for 2 s every 2 min the rate of blockade was more rapid than in unstimulated preparations, similarly 20 mM potassium in the bathing fluid enhanced the rate of blockade.

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