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. 1978 Jul;63(3):551–559. doi: 10.1111/j.1476-5381.1978.tb07811.x

Effect of Crotamine, a Toxin of South American Rattlesnake Venom, on the Sodium Channel of Murine Skeletal Muscle

C Chiung Chang, K Hong Tseng
PMCID: PMC1668090  PMID: 667499

Abstract

1 Crotamine (0.5 μg/ml) augmented the single twitch response of the rat and mouse isolated diaphragm to direct stimulation and prolonged the time course of contraction. At higher doses (10 to 50 μg/ml), contracture was observed with spontaneous fibrillation.

2 The resting membrane potential of diaphragm was rapidly depolarized to about -50 mV within 5 minutes. No increase of depolarization occurred on prolongation of the incubation time or increase of crotamine concentration from 0.5 μg/ml to 50 μg/ml. The effect was not reversed by washing.

3 Tetrodotoxin, low Na+ (12 mM), Ca2+ (10 mM) and procaine (1 mM) prevented the crotamine-depolarization. However, depolarization resumed when crotamine and the antagonists were removed.

4 Low Cl- (8.5 mM) and pretreatment with ouabain enhanced depolarization by crotamine.

5 High K+ (25 to 50 mM) prevented the further depolarization by crotamine and the membrane potential was restored to normal on washout of crotamine with normal Tyrode solution.

6 Effective membrane resistance was decreased by about 50% by crotamine.

7 24Na-influx of the rat diaphragm was increased by crotamine. 42K-influx was slightly increased if tetrodotoxin was also present but was decreased in the absence of tetrodotoxin.

8 No effect on the miniature and evoked endplate potential of the rat diaphragm was observed. Skeletal muscles from frog and chick were not affected.

9 It is inferred that crotamine acts on a molecule regulating the Na+ - permeability of the Na+ channel of murine muscles. It is proposed that extracellular K+ depresses the permeability of the Na+ channel by acting on the same regulator molecule.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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