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It is well established that the respiratory failure caused by cobra venom in dogs and rabbits is due to its peripheral curare-like action (Kellaway, Cherry Lee Vick, Ciuchta & Polley, 1965).Su (1960) has concluded that the neuromuscular blocking effect of the Formosan cobra (Naja naja atra) venom is mainly due to non-depolarizing curare-like action, but is complicated with a direct musculotropic effect, probably due to other components than its neurotoxin.Recently, Su, Chang & Lee (1966) have analysed this problem again with a purified neurotoxin isolated electro- phoretically from this venom.In contrast to the crude venom, the purified neurotoxin blocks neuromuscular transmission by competing with acetylcholine (ACh), without affecting the release of ACh on nerve stimulation in the rat phrenic nerve-diaphragm preparation or causing contracture of the chick biventer cervicis or frog rectus abdominis muscle.These findings led them to conclude that cobra neurotoxin behaves just like d-tubocurarine, although the former agent acts much more slowly and less reversibly than the latter.On the other hand, Meldrum (1965a) isolated component(s) by electrophoresis from Indian cobra venom (Naja naja), which possessed most of the toxicity of the original venom and also depolarized the frog sartorius muscle.It was of interest therefore to study neurotoxin, the major toxic component of Formosan cobra venom, with electro- physiological techniques, in order to clarify the exact mechanism of action.The results so obtained are in good agreement with our previous conclusion that cobra neurotoxin acts quite similarly with d-tubocurarine and indicate that depolarization induced by Meldrum's neurotoxic fraction might be due to incomplete separation from other depolarizing component(s), such as cardiotoxin. METHODS Cobra neurotoxinThis was prepared by either ammonium sulphate precipitation (70-95% saturation) or starch zone electrophoresis as described by Su, Chang & Lee (1966).For the convenience of comparison, the pattern of protein distribution on electrophoresis is shown in Fig. 1.As reported previously, the neurotoxin was located on Peak II while phospholipase A activity and the cardiotoxic component
Chang et al. (Tue,) studied this question.