Soeda Y, O'Brien R D, Yeh J Z, Narahashi T
J Membr Biol. 1975 Aug 11;23(1):91-101. doi: 10.1007/BF01870246.
The basis for the ability of alpha-dihydrograyanotoxin II (alpha-2HG-II) to promote Na+ conductance in axons was sought. The apparent binding of tritiated alpha-2HG-II to neural and other preparations was studied, using equilibrium dialysis, with lobster axon membranes, Torpedo electroplax, housefly head, and rat brain, liver and kidney. In every case the "binding" was nonsaturating and was suggested to involve nonspecific partitioning into the tissue. Supporting evidence was the similarity of extent of "binding" in all tissues and its relative insensitivity to neuropharmacological agents. Alpha-2HG-II did not affect the Na+ conductance of phospholipid bilayers, nor did it permit transport of 22Na into a bulk organic phase. It was concluded that alpha-2HG-II did not bind to the sodium gate, but possibly to a sodium permease present at a frequency of less than one per mu2 of cell membrane.
研究了α-二氢灰毒素II（α-2HG-II）促进轴突中Na+电导能力的基础。使用平衡透析法，以龙虾轴突膜、电鳐电器官、家蝇头部以及大鼠脑、肝和肾为材料，研究了氚标记的α-2HG-II与神经及其他制剂的表观结合情况。在每种情况下，“结合”均不饱和，提示其涉及非特异性分配进入组织。支持证据包括所有组织中“结合”程度的相似性及其对神经药理学试剂的相对不敏感性。α-2HG-II不影响磷脂双层的Na+电导，也不允许22Na转运至大量有机相中。得出的结论是，α-2HG-II不与钠通道结合，而是可能与存在频率低于每μm2细胞膜一个的钠通透酶结合。
