ENHANCEMENT BY AN ANTAGONIST OF TRANSMITTER RELEASE FROM FROG MOTOR NERVE TERMINALS

E. M. SILINSKY*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

The effect of Ba2+ on the synchronous release of acetylcholine from frog motor nerve terminals was studied by conventional electrophysiological techniques. When Ca2+ and Ba2+ were the only divalent cations in the bathing fluid, Ba2+ caused a presynaptic reduction in the amplitude of the endplate potential (e.p.p.). This effect was surmountable by increasing the Ca2+ concentration. The affinity constant (KA) for Ba2+, calculated on the assumption that Ba2+ is a competitive inhibitor of the agonist, Ca2+, was 1.1 + 0.4 mM−1 (mean + s.e.mean, n = 8). When e.p.ps were depressed by the addition of 1 mm Mg2+, addition of Ba2+ (1 to 3 mm) caused either a further presynaptic depression of moderate magnitude or had no additional effect. When e.p.p.s were depressed with [Mg2+] > 2 mm, addition of Ba2+ > 0.9 mm enhanced the e.p.p. amplitude by a presynaptic mechanism. The interaction of the divalent cation antagonists Mg2+ and Ba2+ with the agonist, Ca2+ is discussed. It is demonstrated that a model which considers the nonequilibrium, kinetic properties of binding can be used to describe interactions between divalent cations at the external surface of the motor nerve ending. 1978 British Pharmacological Society

Original languageEnglish (US)
Pages (from-to)485-493
Number of pages9
JournalBritish journal of pharmacology
Volume63
Issue number3
DOIs
StatePublished - Jul 1978

ASJC Scopus subject areas

  • Pharmacology

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