海葵毒素与小龙虾巨轴突中钠通道的结合特性。

Binding properties of sea anemone toxins to sodium channels in the crayfish giant axon.

Warashina A, Ogura T, Fujita S

Department of Physiology, Niigata University School of Medicine, Japan.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1988;90(2):351-9.

Abstract

Effects of four different sea anemone toxins from Anthopleura (AP-A and AP-C), Anemonia (ATX II) and Parasicyonis (PaTX), and a scorpion toxin from Leiurus (LqTX) on crayfish giant axons were studied. 2. These toxins slowed the Na channel inactivation process, inducing a maintained Na current during a depolarizing pulse. 3. The binding rates for these toxins markedly decreased under depolarization. The decrease in AP-A binding was mainly derived from an increased dissociation rate under depolarization whereas that in PaTX binding from a reduced association rate. 4. The potential-dependent toxin binding kinetics seemed to be related to the gating mechanism of the Na channel. 5. Competitive bindings between these toxins were demonstrated.

摘要

研究了来自海葵属的四种不同海葵毒素（AP - A和AP - C）、海葵毒素（ATX II）和副侧花海葵毒素（PaTX）以及来自金蝎属的一种蝎毒素（LqTX）对小龙虾巨轴突的影响。2. 这些毒素减缓了钠通道失活过程，在去极化脉冲期间诱导持续的钠电流。3. 在去极化条件下，这些毒素的结合速率显著降低。AP - A结合的降低主要源于去极化时解离速率的增加，而PaTX结合的降低源于结合速率的降低。4. 电位依赖性毒素结合动力学似乎与钠通道的门控机制有关。5. 证明了这些毒素之间的竞争性结合。