Barton S B, Cohen I S
Pflugers Arch. 1982 Feb;392(4):327-34. doi: 10.1007/BF00581627.
Exposure of frog neuromuscular junctions to solutions which contain a high concentration of calcium ions produces failure of neuromuscular transmission. This failure of transmission is abrupt and usually complete. However, some terminals produce small end-plate potentials even after the exposure to a high concentration of calcium ions. A second stimulus to the nerve can overcome the block of neuromuscular transmission if the interval between the stimuli is less than a critical value. The size of the end-plate potential is almost independent of the interstimulus interval if the latter is less than the critical value but more than the refractory period. The depth of this neuromuscular block is affected by temperature, potassium ions, osmotic pressure, cobalt ions, and prior high frequency stimulation of the nerve. Neuromuscular transmission failure coincides with failure of the nerve action potential (NAP) to invade the terminal. Prior to propagation failure, the second extracellularly recorded NAP is smaller, but is conducted faster than the first NAP. The relevance of these findings to the facilitation of transmitter release seen in solutions of normal divalent ion content is discussed.
将青蛙神经肌肉接头暴露于含有高浓度钙离子的溶液中会导致神经肌肉传递失败。这种传递失败是突然的,通常是完全的。然而,即使在暴露于高浓度钙离子后,一些终末仍会产生小的终板电位。如果两次刺激之间的间隔小于临界值,对神经的第二次刺激可以克服神经肌肉传递的阻断。如果刺激间隔小于临界值但大于不应期,终板电位的大小几乎与刺激间隔无关。这种神经肌肉阻断的深度受温度、钾离子、渗透压、钴离子以及先前对神经的高频刺激影响。神经肌肉传递失败与神经动作电位(NAP)无法侵入终末同时发生。在传播失败之前,细胞外记录的第二个NAP较小,但传导速度比第一个NAP快。讨论了这些发现与在正常二价离子含量溶液中观察到的递质释放促进作用的相关性。