Abstract

1. 1.|The suppression of the propagated action potential in the squid giant axon and in the frog sciatic nerve, by saturated solutions of the n-alkanes from n-pentane to n-decane, has been examined. A progressive loss inthe activity of the alkane was found as the chain length increased, n-nonane being effectively inert. The concentration dependence of the suppression of the action potentially n-pentane was also measured. 2. 2.|The effects of the alkanes on lipid bilayers were determined using black film techniques. For both phosphatidylcholine-cholesterol and monoolein-cholesterol bilayers in alkane-saturated aqueous phases, the bilayer thickness decreased by several angstrom units on passing from n-pentane to n-decane, from which it was conclude that the adsorption also decreased. The concentration dependence of the thickness and adsorption changes for n-pentane were examined. 3. 3.|A close correlation is shown to exist between the nerve results and those for a phosphaytidylcholine-cholesterol bilayer, suggesting that the site of action of the alkane is in a lipid bilayer region of the nerve mumbrane. 4. 4.|The presence of cholesterol in the bilayer, at levels apparently comparable to those in axon membranes, is essentiol for the above correlation to hold. 5. 5.|A molecular mechanism by which the alkane may inhibit the nerve impulse is proposed. The essential feature is that a thickening of the lipid part of an axon mumbrane through adsorption of alkane reduces the stability of the ionic channels formed during electrical excitation.

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