Molgo J, Lemeignan M, Lechat P
J Pharmacol Exp Ther. 1977 Dec;203(3):653-63.
Micromolar concentrations of 4-aminopyridine (4-AP) were able to increase the amplitude of the end-plate current in frog neuromuscular junction blocked either by d-tubocurarine or by low Ca++ high Mg++ medium. The end-plate potential was also increased. These effects were reversible. The changes in the end-plate current amplitude observed after 4-AP treatment had no effect on the end-plate current time course. There was no significant difference in the resting membrane potential or mean amplitude and frequency of spontaneous miniature end-plate potentials in the presence of 4-AP. The quantal content of the end-plate potential was increased in every preparation tested and the minimal synpatic delay was lengthened in a dose-related way. 4-AP did not modify the dependence of the amplitude of the end-plate current on membrane potential. In the presence of 4-AP, the time constant of the falling phase of the end-plate current remained an exponential function of the membrane potential. The end-plate current equilibrium potential was unaffected by 4-AP. The increase in the amount of acetylcholine released by nerve impulse induced by 4-AP occurs without modification in the calcium cooperativity. The authors suggest that 4-AP, by prolonging the presynaptic action potential, could increase calcium concentration in the nerve terminal and, thus, the transmitter release.
微摩尔浓度的4-氨基吡啶（4-AP）能够增加被d-筒箭毒碱或低钙高镁培养基阻断的青蛙神经肌肉接头处终板电流的幅度。终板电位也增加了。这些效应是可逆的。4-AP处理后观察到的终板电流幅度变化对终板电流的时间进程没有影响。在存在4-AP的情况下，静息膜电位或自发微小终板电位的平均幅度和频率没有显著差异。在每个测试的标本中，终板电位的量子含量增加，最小突触延迟以剂量相关的方式延长。4-AP没有改变终板电流幅度对膜电位的依赖性。在存在4-AP的情况下，终板电流下降相的时间常数仍然是膜电位的指数函数。终板电流平衡电位不受4-AP的影响。4-AP诱导的神经冲动释放的乙酰胆碱量的增加在钙协同作用没有改变的情况下发生。作者认为，4-AP通过延长突触前动作电位，可以增加神经末梢中的钙浓度，从而增加递质释放。
