Bradley R J, Edge M T, Chau W C
Department of Psychiatry, School of Medicine, University of Alabama, Birmingham 35294.
Eur J Pharmacol. 1990 Jan 25;176(1):11-21. doi: 10.1016/0014-2999(90)90127-r.
d-Tubocurarine and the alpha-neurotoxins from snake venom are antagonists at the nicotinic acetylcholine receptor. It is well established that d-tubocurarine causes fade in neuromuscular transmission during repetitive nerve stimulation but paradoxically there are many reports which indicate that the alpha-neurotoxins do not cause such fade. We found that high concentrations of erabutoxin b (100-150 nM) from the venom of Laticauda semifasciata did not cause much fade in the rat diaphragm preparation. However, low concentrations of toxin (5 nM) caused severe fade which was similar to the effects of d-tubocurarine. The data suggest that fade may be caused by toxin binding to a high-affinity site on the postsynaptic acetylcholine receptor.
筒箭毒碱和蛇毒中的α-神经毒素是烟碱型乙酰胆碱受体的拮抗剂。众所周知,筒箭毒碱在重复神经刺激期间会导致神经肌肉传递出现衰减,但矛盾的是,有许多报告表明α-神经毒素不会引起这种衰减。我们发现,来自半环扁尾海蛇毒液的高浓度 erabutoxin b(100 - 150 nM)在大鼠膈肌标本中不会引起太多衰减。然而,低浓度的毒素(5 nM)会导致严重衰减,这与筒箭毒碱的作用相似。数据表明,衰减可能是由于毒素与突触后乙酰胆碱受体上的高亲和力位点结合所致。