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The Journal of General Physiology, Vol 58, 413-437, Copyright © 1971 by The Rockefeller University Press


ARTICLE

Interaction of Tetraethylammonium Ion Derivatives with the Potassium Channels of Giant Axons

Clay M. Armstrong 1

1 From the Department of Physiology, University of Rochester School of Medicine and Dentistry, Rochester, New York 14620, and the Laboratorio de Fisiologia Celular, Montemar, Chile

A number of compounds related to TEA+ (tetraethylammoniumion) were injected into squid axons and their effects on gK (the potassium conductance) were determined. In most of these ions a quaternary nitrogen is surrounded by three ethyl groups and a fourth group that is very hydrophobic. Several of the ions cause inactivation of gK, a type of ionic gating that is not normally seen in squid axon; i.e., after depolarization gK increases and then spontaneously decreases to a small fraction of its peak value even though the depolarization is maintained. Observations on the mechanism of this gating show that (a) QA (quaternary ammonium) ions only enter K+ channels that have open activation gates (the normal permeability gates). (b) The activation gates of QA-occluded channels do not close readily. (c) Hyperpolarization helps to clear QA ions from the channels. (d) Raising the external K+ concentration also helps to clear QA ions from the channels. Observations (c) and (d) strongly suggest that K+ ions traverse the membrane by way of pores, and they cannot be explained by the usual type of carrier model. The data suggest that a K+ pore has two distinct parts: a wide inner mouth that can accept a hydrated K+ ion or a TEA+-like ion, and a narrower portion that can accept a dehydrated or partially dehydrated K+ ion, but not TEA+.

Submitted on March 31, 1971


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