Time course of TEA(+)-induced anomalous rectification in squid giant axons.
Changes in the voltage clamp currents of squid giant axons wrought by low axoplasmic TEA+ (tetraethylammonium chloride) concentrations (0.3 mM and above) are described. They are: (a) For positive steps from the resting potential in sea water, the K+ current increases, decreases, then increases, instead of increasing monotonically. (b) For positive steps from the resting potential in 440 mM external K+, the current has an exponentially decaying component, whose decay rate increases with axoplasmic [TEA+]. The control currents increase monotonically. (c) For negative steps from the resting potential in 440 mM external K+, the current record has a peak followed by a decay that is slow relative to the control. The control record decreases monotonically. Qualitatively these findings can be described by a simple kinetic model, from which, with one assumption, it is possible to calculate the rate at which K+ ions move through the K+ channels. An interesting conclusion from (c) is that the channels cannot be closed by the normal voltage-sensitive mechanism (described by Hodgkin and Huxley) until they are free of TEA+.
Armstrong
C M
CM
National Institutes of Health, Bethesda, Maryland, USA.
D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology*; D000818:Animals; D001369:Axons / Q000502:physiology*; D049832:Decapodiformes; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008954:Models, Biological; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D011930:Reaction Time / Q000502:physiology; D019789:Tetraethylammonium / Q000494:pharmacology*
D019789:Tetraethylammonium; D011188:Potassium