Effects of venoms on the squid giant axon

Abstract

Tiger snake venom was the most potent of 9 venoms tested in its ability to render the squid giant axon reactive to d-tubocurarine (curare); its potency in this regard is about equal to that of cottonmouth moccasin venom which was the most potent venom previously found. Timber rattlesnake, sea snake, scorpion, and yellow hornet venom and a component from cobra venom referred to as neurotoxin were completely inactive. These results are in agreement with the hypothesis that phospholipase A is the component of venoms responsible for reducing the permeability barriers, surrounding the excitable membrane of squid axons, to acetylcholine (ACh) and curare, thereby allowing them to interact with the ACh receptors in the conducting membrane and block electrical activity. Neuraminidase, saponin, arsenite, veratridine, NN-dimethylformamide, dimethyl sulfoxide and histamine failed to render the axon responsive to the action of curare. Venoms and the cationic detergent cetyltrimethylammonium remain as the only compounds found so far which are effective in altering the structural permeability barriers surrounding the excitable membrane of the squid giant axon.