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. 1983 May;79(1):201–209. doi: 10.1111/j.1476-5381.1983.tb10513.x

Extracellular chloride replacement by isethionate induces abnormal spontaneous release of transmitter at the frog neuromuscular junction.

M L Ashford, K T Wann
PMCID: PMC2044824  PMID: 6135475

Abstract

1 Replacement of chloride by isethionate in Ringer solution bathing frog skeletal muscle fibres induces, after a delay of about 30 min, marked mechanical activity which was blocked by tubocurarine. This effect is reversed by washing out the isethionate. 2 Miniature end plate potentials (m.e.p.ps) and giant potentials (potentials greater than or equal to 2 X modal value) were recorded intracellularly in normal Ringer and isethionate Ringer solution. 3 The frequency of m.e.p.ps was unaltered by isethionate. The proportion of giant potentials increased from 3% in normal Ringer to 24.5% in isethionate Ringer after 90 min. This effect is usually reversible if the exposure to isethionate does not exceed 2 h. 4 The giant potentials were large enough to initiate trains of action potentials and still occurred in the presence of tetrodotoxin or Ca2+-free Ringer. Isethionate produced no change in the tau D of miniature endplate currents. 5 Chloride replacement by propionate produced no change in the proportion of giant potentials. 6 It is suggested that the isethionate anion can induce giant potentials and the possible mechanism of action is discussed.

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Selected References

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