Muramatsu I, Saito K, Ohmura T, Kigoshi S, Shibata S
Department of Pharmacology, Fukui Medical School, Japan.
Eur J Pharmacol. 1990 Sep 4;186(1):41-7. doi: 10.1016/0014-2999(90)94058-6.
Anthopleurin-A produced two distinct responses in crayfish giant axons: depolarization and prolongation of action potentials. The depolarization was prominent at low concentrations of anthopleurin-A, while a remarkable prolongation of the action potential was produced by higher concentrations of anthopleurin-A. Both effects of anthopleurin-A were inhibited by pre- or posttreatment with tetrodotoxin or lidocaine at concentrations which had not effect on the normal sodium channel. The prolongation of the action potential was more sensitive to tetrodotoxin and lidocaine than the depolarization was. These results suggest that sodium channels of the crayfish giant axon are modified by anthopleurin-A in at least two ways, thereby resulting in sensitization to tetrodotoxin and lidocaine.
海葵毒素 - A在小龙虾巨轴突中产生两种不同的反应：动作电位的去极化和延长。在低浓度的海葵毒素 - A下，去极化现象显著，而高浓度的海葵毒素 - A则会使动作电位明显延长。海葵毒素 - A的这两种效应在使用对正常钠通道无影响浓度的河豚毒素或利多卡因进行预处理或后处理时均受到抑制。动作电位的延长比去极化对河豚毒素和利多卡因更敏感。这些结果表明，小龙虾巨轴突的钠通道至少通过两种方式被海葵毒素 - A修饰，从而导致对河豚毒素和利多卡因敏感。
