Krueger B K, Blaustein M P, Ratzlaff R W
J Gen Physiol. 1980 Sep;76(3):287-313. doi: 10.1085/jgp.76.3.287.
Regulation of Na+ channels by neurotoxins has been studied in pinched-off nerve endings (synaptosomes) from rat brain. Activation of Na+ channels by the steroid batrachotoxin and by the alkaloid veratridine resulted in an increase in the rate of influx of 22Na into the synaptosomes. In the presence of 145 mM Na+, these agents also depolarized the synaptosomes, as indicated by increased fluorescence in the presence of a voltage-sensitive oxacarbocyanine dye [diO-C5(3)]. Polypeptide neurotoxins from the scorpion Leiurus quinquestriatus and from the sea anemone Anthopleura xanthogrammica potentiated the stimulatory effects of batrachotoxin and veratridine on the influx of 22Na into synaptosomes. Saxitoxin and tetrodotoxin blocked the stimulatory effects of batrachotoxin and veratridine, both in the presence and absence of the polypeptide toxins, but did not affect control 22Na influx or resting membrane potential. A three-state model for Na+ channel operation can account for the effects of these neurotoxins on Na+ channels as determined both by Na+ flux measurements in vitro and by electrophysiological experiments in intact nerve and muscle.
已经在大鼠脑的分离神经末梢（突触体）中研究了神经毒素对钠离子通道的调节作用。甾体类毒素箭毒蛙毒素和生物碱藜芦定激活钠离子通道，导致突触体中22Na流入速率增加。在含有145 mM Na+的情况下，这些物质还使突触体去极化，这可通过电压敏感性羰花青染料[二氧杂羰花青C5(3)]存在时荧光增强来表明。来自以色列金蝎和黄海葵的多肽神经毒素增强了箭毒蛙毒素和藜芦定对突触体中22Na流入的刺激作用。在存在和不存在多肽毒素的情况下，石房蛤毒素和河豚毒素均阻断箭毒蛙毒素和藜芦定的刺激作用，但不影响对照22Na流入或静息膜电位。钠离子通道运作的三态模型可以解释这些神经毒素对钠离子通道的作用，这是通过体外钠离子通量测量以及完整神经和肌肉中的电生理实验确定的。
