Evidence that α-dihydrograyanotoxin II does not bind to the sodium gate

The basis for the ability of α-dihydrograyanotoxin II (α-2HG-II) to promote Na⁺ conductance in axons was sought. The apparent binding of tritiated α-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. α-2HG-II did not affect the Na⁺ conductance of phospholipid bilayers, nor did it permit transport of²²Na into a bulk organic phase. It was concluded that α-2HG-II did not bind to the sodium gate, but possibly to a sodium permease present at a frequency of less than one per μ² of cell membrane.