Reversible block of axonal conduction by curare after treatment with cobra venom

Abstract

After treatment of squid giant axon with cobra venom (CV), cetyltrimethyl-ammonium chloride (CTA) or a combination of the two, d-tubocurarine (curare) caused reversible block of conduction at concentrations as low as 5 × 10−4 M. On control axons, 1.4 × 10−2 M curare had little effect on electrical activity. Other compounds rendered active by the treatment included chlorisondamine and protamine; the actions of physostigmine and diisopropylfluorophosphate were potentiated. Several quaternary ammonium compounds, among them prostigmine and acetylcholine, were not rendered active after pretreatment. Most tertiary amines affected the untreated squid axon action potential in almost the same concentrations that affect the synapses of the single electroplax. In contrast to lipid-insoluble quaternary ammonium compounds, which did not significantly alter the action potential of the untreated axon, three lipid-soluble quaternary compounds were as effective on the axon as on other conducting membranes. The results indicate that a strong lipid barrier surrounds the squid axon. A mechanism for the breakdown of this barrier by CV and CTA is discussed. Possible explanations are presented for the inability of this treatment to permit effects of some lipid insoluble quaternary compounds.