Sano K, Enomoto K, Maeno T
Department of Internal Medicine, Shimane Medical University, Japan.
Eur J Pharmacol. 1987 Sep 11;141(2):235-41. doi: 10.1016/0014-2999(87)90268-8.
A new type Ca2+ antagonist, synthetic omega-conotoxin (omega-CgTX) decreased the peak height of the endplate potential (EPP) in frog muscle but had no effect on the mouse neuromuscular junction. The reduction of endplate potential in frogs was due to a decrease in transmitter release, since the mean quantal content estimated by variance of EPPs (m) and from the peak heights of EPPs and miniature EPPs (m1) was reduced by omega-CgTX, but the postsynaptic sensitivity to ACh was unaltered. The decrease of mean quantal content caused by omega-CgTX was reversed by 4-aminopyridine, guanidine and Bay K 8644. Also, the effect of omega-CgTX was weakened in the presence of 10 mM Ca2+ or 12 mM Mg2+. Statistical analysis revealed that omega-CgTX decreased the number of quanta available (n) whereas the probability of release (p) remained unaffected.
一种新型钙离子拮抗剂，合成的ω-芋螺毒素（ω-CgTX）可降低蛙肌终板电位（EPP）的峰值高度，但对小鼠神经肌肉接头无影响。蛙终板电位的降低是由于递质释放减少所致，因为通过EPPs的方差估计的平均量子含量（m）以及从EPPs和微小EPPs的峰值高度估计的平均量子含量（m1）均被ω-CgTX降低，但突触后对乙酰胆碱的敏感性未改变。ω-CgTX引起的平均量子含量降低可被4-氨基吡啶、胍和Bay K 8644逆转。此外，在10 mM钙离子或12 mM镁离子存在的情况下，ω-CgTX的作用会减弱。统计分析表明，ω-CgTX减少了可用量子的数量（n），而释放概率（p）保持不变。
