Yu S P, Van der Kloot W
Department of Physiology, Health Sciences Center, SUNY, Stony Brook 11794.
Neurosci Lett. 1990 Sep 4;117(1-2):111-6. doi: 10.1016/0304-3940(90)90128-v.
The rate of non-quantal acetylcholine (ACh) release was estimated at the mouse neuromuscular junction by observing the effect of (+)-tubocurarine on endplate membrane potential or current in preparations pretreated with an irreversible anti-acetylcholinesterase (anti-AChE). Voltage clamping was an effective method for measuring non-quantal release. Non-quantal release was markedly inhibited by 10 microM aconitine. Non-quantal release was not significantly increased by 10 microM dihyroouabain (DHO). (It has been reported that ouabain increases the leak). Non-quantal release was roughly doubled following exposure to hypertonic solution or to elevated K(+)-solution. This is in accord with the hypothesis that the leak is by way of ACh transporters incorporated into the terminal membrane following exocytosis, but other interpretations remain to be tested.
通过观察（+）-筒箭毒碱对用不可逆抗乙酰胆碱酯酶（抗AChE）预处理的标本中终板膜电位或电流的影响，估算了小鼠神经肌肉接头处非量子化乙酰胆碱（ACh）的释放速率。电压钳制是测量非量子化释放的有效方法。10μM乌头碱可显著抑制非量子化释放。10μM双氢哇巴因（DHO）不会使非量子化释放显著增加。（据报道哇巴因会增加泄漏）。暴露于高渗溶液或高钾溶液后，非量子化释放大致增加一倍。这与以下假设一致，即泄漏是通过胞吐作用后整合到终末膜中的ACh转运体进行的，但其他解释仍有待检验。
