Worley J F, French R J, Krueger B K
J Gen Physiol. 1986 Feb;87(2):327-49. doi: 10.1085/jgp.87.2.327.
Single batrachotoxin-activated sodium channels from rat brain were modified by trimethyloxonium (TMO) after incorporation in planar lipid bilayers. TMO modification eliminated saxitoxin (STX) sensitivity, reduced the single channel conductance by 37%, and reduced calcium block of inward sodium currents. These effects always occurred concomitantly, in an all-or-none fashion. Calcium and STX protected sodium channels from TMO modification with potencies similar to their affinities for block. Calcium inhibited STX binding to rat brain membrane vesicles and relieved toxin block of channels in bilayers, apparently by competing with STX for the toxin binding site. These results suggest that toxins, permeant cations, and blocking cations can interact with a common site on the sodium channel near the extracellular surface. It is likely that permeant cations transiently bind to this superficial site, as the first of several steps in passing inward through the channel.
将大鼠脑内的单个蛙毒素激活的钠通道整合到平面脂质双分子层后，用三甲基氧鎓（TMO）进行修饰。TMO修饰消除了石房蛤毒素（STX）敏感性，使单通道电导降低37%，并减少了内向钠电流的钙阻滞。这些效应总是同时以全或无的方式出现。钙和STX对钠通道具有保护作用，使其免受TMO修饰，其效力与其对通道阻滞的亲和力相似。钙抑制STX与大鼠脑膜囊泡的结合，并解除双层膜中通道的毒素阻滞，显然是通过与STX竞争毒素结合位点来实现的。这些结果表明，毒素、通透阳离子和阻滞阳离子可以与细胞外表面附近钠通道上的一个共同位点相互作用。通透阳离子很可能短暂地结合到这个表面位点，这是其向内穿过通道的几个步骤中的第一步。
