Tabti N, Lupa M T, Yu S P, Thesleff S
Acta Physiol Scand. 1986 Nov;128(3):429-36. doi: 10.1111/j.1748-1716.1986.tb07996.x.
A variety of pharmacologically active compounds was surveyed for effects on the Ca2+-insensitive miniature end-plate potentials (slow mepps) induced by botulinum toxin type A (Botx) poisoning in rat muscle. The purpose was to gain insight into the release process responsible for this type of acetylcholine secretion. It was found that caffeine and dibutyryl cyclic adenosine 3',5'-monophosphate increased significantly the frequency of slow mepps in Botx-poisoned muscles, but had no effect on slow mepps in control muscles. Vinblastine and cytochalasin B significantly increased the slow mepp frequency in Botx-poisoned as well as in normal control muscles. Inhibitors of oxidative metabolism reduced the frequency of slow mepps by 90%, indicating a high energy requirement for this type of release. No agent was found to augment the slow mepp frequency above 1-2 Hz, suggesting that an upper limit exists for this type of packaging and release of acetylcholine.
研究了多种药理活性化合物对A型肉毒杆菌毒素（Botx）中毒大鼠肌肉中钙不敏感型微小终板电位（慢微小终板电位）的影响。目的是深入了解导致此类乙酰胆碱分泌的释放过程。结果发现，咖啡因和二丁酰环腺苷3',5'-单磷酸显著增加了Botx中毒肌肉中慢微小终板电位的频率，但对对照肌肉中的慢微小终板电位没有影响。长春碱和细胞松弛素B显著增加了Botx中毒肌肉以及正常对照肌肉中的慢微小终板电位频率。氧化代谢抑制剂使慢微小终板电位的频率降低了90%，表明此类释放需要高能量。未发现任何药剂能将慢微小终板电位频率提高到1-2Hz以上，这表明此类乙酰胆碱的包装和释放存在上限。
