Inactivation of the Potassium Conductance and Related Phenomena Caused by Quaternary Ammonium Ion Injection in Squid Axons (original) (raw)

J Gen Physiol. 1969 Nov 1; 54(5): 553–575.

From the Departments of Physiology and Neurology, Duke University Medical Center, Durham, North Carolina 27706, and Laboratorio de Fisiología Celular, Montemar, Chile.

Dr. Armstrong's present address is Department of Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14620

Copyright © 1969 by The Rockefeller University Press

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Abstract

Several analogues of the tetraethylammonium (TEA+) ion were injected into the giant axon of the squid, and the resultant changes in time course and magnitude of the potassium current (I K) were studied. For all the analogues used, three of the ethyl side chains of TEA+ were left unchanged, while the fourth chain was either lengthened or shortened. Increasing the length of this chain increased binding to the blocking site in the channel by a factor of roughly two for each added CH2 group. The effect on the rate of entry into the blocking site was relatively slight. Thus the concentration for half-suppression of g K decreased by about the same factor of two for each added CH2. All the analogues caused anomalous or ingoing rectification. The longest chain analogue used, pentyltriethylammonium ion, caused rapid inactivation of g K, and this inactivation had properties quite similar to g Na inactivation. The anomalous rectification and the g K inactivation caused by these compounds have the same basic mechanism.

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