Katz B, Miledi R
Proc R Soc Lond B Biol Sci. 1981 May 7;212(1186):131-7. doi: 10.1098/rspb.1981.0029.
Previous experiments have indicated that there is a continuous leakage of acetylcholine (ACh) from resting motor nerve terminals which can produce a small depolarization in anti-esterase treated endplates (Katz & Miledi 1977; Vyskocil & Illés 1978). This leakage might be expected to be intensified during the presynaptic action potential and also lead to a very small non-quantal endplate response. This hypothesis was examined, in frog and mammalian endplates, by stimulating the motor nerve in a calcium-deprived medium and recording the summated average response to several hundred stimuli. The result was completely negative; no trace of a non-quantal endplate potential was ever observed, with the limit of detection being always less than 10 microV, and sometimes as low as 2 microV. These experiments suggest that the leakage of ACh either does not originate predominantly from the synaptic region of the axon terminal, or that it occurs by a mechanism that is not directly influenced by the membrane potential.
先前的实验表明，静息运动神经末梢会持续释放乙酰胆碱（ACh），这会在抗酯酶处理的终板中产生微小的去极化（Katz和Miledi，1977年；Vyskocil和Illés，1978年）。预计这种释放在突触前动作电位期间会增强，并且还会导致非常小的非量子化终板反应。在青蛙和哺乳动物的终板中，通过在缺钙培养基中刺激运动神经并记录对数百次刺激的总和平均反应，对这一假设进行了检验。结果完全是否定的；从未观察到非量子化终板电位的迹象，检测极限始终小于10微伏，有时低至2微伏。这些实验表明，乙酰胆碱的释放要么主要不是源自轴突末梢的突触区域，要么其发生机制不受膜电位的直接影响。
