EFFECTS OF 4-AMINOPYRIDINE AT FROG NEUROMUSCULAR-JUNCTION

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 203  (3) , 653-663
Abstract
Micromolar concentrations of 4-aminopyridine (4-AP) were able to increase the amplitude of the endplate current in frog [Rana esculenta] neuromuscular junction blocked either by d-tubocurarine or by low Ca2+ high Mg2+ medium. The endplate potential was also increased. These effects were reversible. The changes in the endplate current amplitude observed after 4-AP treatment had no effect on the endplate current time course. There was no significant difference in the resting membrane potential or mean amplitude and frequency of spontaneous miniature endplate potentials in the presence of 4-AP. The quantal content of the endplate potential was increased in every preparation tested and the minimal synaptic delay was lengthened in a dose-related way. 4-AP did not modify the dependence of the amplitude of the endplate current on membrane potential. In the presence of 4-AP, the time constant of the falling phase of the endplate current remained an exponential function of the membrane otential. The endplate current equilibrium potential was unaffected by 4-AP. The increase in the amount of acetylcholine released by nerve impulse induced by 4-AP occurred without modification in the Ca2+ cooperativity. 4-AP, by prolonging the presynaptic action potential, could increase Ca2+ concentration in the nerve terminal and, thus, the transmitter release.