Zushi S, Miyagawa J, Yamamoto M, Kataoka K, Seyama I
J Pharmacol Exp Ther. 1983 Jul;226(1):269-75.
The effect of alpha-dihydrograyanotoxin II (alpha-H2-GTX II) on the neuromuscular junction of the frog was examined by the intracellular microelectrode technique. alpha-H2-GTX II (6 microM), with a latency of about 20 min, caused a depolarization of both the end-plate and non-end-plate region of the muscle fiber. Concomitantly, alpha-H2-GTX II caused a marked increase in the frequency of m.e.p.p.s, which persisted for 1 hr; thereafter m.e.p.p.s were gradually abolished. In end-plates which had become quiescent after treatment with alpha-H2-GTX II, synaptic vesicles could no longer be recognized histologically, suggesting that alpha-H2-GTX II depleted the store of vesicles. alpha-H2-GTX II did not affect the iontophoretically evoked acetylcholine potential, suggesting that the toxin did not greatly alter the sensitivity of the end-plate membrane to acetylcholine. Removal of Ca++ from the external medium prevented alpha-H2-GTX II from discharging synaptic vesicles. Application of tetrodotoxin or removal of Na+ ions before exposure to alpha-H2-GTX II prevented both the toxin-induced depolarization and increase in m.e.p.p. frequency. It is concluded that the action of GTX on the neuromuscular junction is probably due to an increase in membrane permeability to Na+, resulting in depolarization of both the presynaptic and postsynaptic membranes.
采用细胞内微电极技术研究了α-二氢灰毒素II（α-H2-GTX II）对青蛙神经肌肉接头的作用。α-H2-GTX II（6微摩尔），潜伏期约20分钟，可引起肌肉纤维终板区和非终板区的去极化。同时，α-H2-GTX II可使微小终板电位（m.e.p.p.s）频率显著增加，持续1小时；此后m.e.p.p.s逐渐消失。在用α-H2-GTX II处理后变得静止的终板中，组织学上已无法识别突触小泡，这表明α-H2-GTX II耗尽了小泡储备。α-H2-GTX II不影响离子电泳诱发的乙酰胆碱电位，提示该毒素并未显著改变终板膜对乙酰胆碱的敏感性。从外部介质中去除Ca++可阻止α-H2-GTX II释放突触小泡。在暴露于α-H2-GTX II之前应用河豚毒素或去除Na+离子可阻止毒素诱导的去极化和m.e.p.p.频率增加。结论是，GTX对神经肌肉接头的作用可能是由于膜对Na+的通透性增加，导致突触前膜和突触后膜去极化。
