X-537A is an ionophore that can carry cations across cell membranes. We studied its effects on spontaneous and stimulated quantal acetylcholine (ACh) release at the frog neuromuscular junction. 2. When neuromuscular transmission was blocked with high Mg2+ or with curare, X-537A markedly increased the end-plate potential (e.p.p.) amplitude. Then a few minutes later the e.p.p. disappeared. 3. When neuromuscular transmission was blocked with hypertonic saline solution, X-537A did not increase e.p.p. amplitude; it did produce many transmission failures. 4. X-537A decreased the depolarization of the end-plate produced by iontophoretically applied ACh. this may account in part for the disappearance of the e.p.p. in solutions containing the ionophore. 5. X-537A depolarized muscle fibres by about 15 mV. 6. When the extracellular divalent cation concentration was very low, X-537A had little or no effect on miniature end-plate potential (min.e.p.p.) frequency. 7. When a divalent cation was present in the extracellular fluid, X-537A increased the frequency of the min.e.p.p.s. The sequence of effectiveness of the divalent ions we have tested is: Ba2+ greater than Sr2+ greater than Ca2+ greater than Mn2+ congruent to Co2+ congruent to Ni2+ greater than Mg2+. There is a rough parallel between these results and the reported affinity of X-537A for various divalent ions. 8. The increase in min.e.p.p. frequency caused by X-537A was transitory, following the increase min.e.p.p. frequency fell to a very low rate or to zero. Then nerve stimulation did not cause quantal release. A second application of X-537A was without effect. 9. X-537A decreased min.e.p.p. amplitude, in accord with the effect on the sensitivity of the end-plate to ACh. 10. The results support the idea that increases in intracellular divalent cation concentrations trigger quantal release from nerve terminals and are involved in the disensitization of end plate receptors to ACh.
摘要
X - 537A是一种离子载体，能够携带阳离子穿过细胞膜。我们研究了它对青蛙神经肌肉接头处自发和刺激诱发的量子化乙酰胆碱（ACh）释放的影响。2. 当用高镁离子或箭毒阻断神经肌肉传递时，X - 537A显著增加终板电位（e.p.p.）的幅度。然后几分钟后终板电位消失。3. 当用高渗盐溶液阻断神经肌肉传递时，X - 537A不会增加终板电位幅度；它确实会导致许多传递失败。4. X - 537A降低了离子电泳施加乙酰胆碱所产生的终板去极化。这可能部分解释了在含有该离子载体的溶液中终板电位消失的原因。5. X - 537A使肌肉纤维去极化约15毫伏。6. 当细胞外二价阳离子浓度非常低时，X - 537A对微小终板电位（min.e.p.p.）频率几乎没有影响。7. 当细胞外液中存在二价阳离子时，X - 537A增加微小终板电位的频率。我们测试的二价离子的有效性顺序是：钡离子大于锶离子大于钙离子大于锰离子等同于钴离子等同于镍离子大于镁离子。这些结果与报道的X - 537A对各种二价离子的亲和力之间存在大致的平行关系。8. X - 537A引起的微小终板电位频率增加是短暂的，频率增加后会降至非常低的速率或变为零。然后神经刺激不会导致量子化释放。再次应用X - 537A没有效果。9. X - 537A降低了微小终板电位幅度，这与对终板对乙酰胆碱敏感性的影响一致。10. 这些结果支持这样一种观点，即细胞内二价阳离子浓度的增加触发神经末梢的量子化释放，并参与终板受体对乙酰胆碱的脱敏作用。
