Enhancement by an antagonist of transmitter release from frog motor nerve terminals.
1 The effect of Ba2+ on the synchronous release of acetylcholine from frog motor nerve terminals was studied by conventional electrophysiological techniques. 2 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. 3 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). 4 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. 5 When e.p.p.s were depressed with [Mg2+] greater than or equal to 2 mM, addition of Ba2+ greater than or equal to 0.9 mM enhanced the e.p.p. amplitude by a presynaptic mechanism. 6 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.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001001:Anura; D001464:Barium / Q000494:pharmacology*; D002118:Calcium / Q000502:physiology; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008274:Magnesium / Q000502:physiology; D009046:Motor Neurons / Q000378:metabolism* / Q000502:physiology; D009411:Nerve Endings / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D011894:Rana pipiens
D018377:Neurotransmitter Agents; D001464:Barium; D008274:Magnesium; D000109:Acetylcholine; D002118:Calcium