Blocking kinetics of the anomalous potassium rectifier of tunicate egg studied by single channel recording

Abstract

1. The kinetics of the anomalous K current produced by blocking cations Na, Cs and Sr were analysed by single channel recording in the tunicate egg cell.2. The open-close kinetics in a single channel with the presence of blocking cation were consistent with the blocking kinetics of the total anomalous K current. The open-close kinetics in a single anomalous K rectifier channel could be regarded as the first order transition between the open and closed states.3. The closing rate constants of the single channel for the first order transition increased almost linearly on a semilogarithmic scale as the membrane potential became more negative, while the opening rate constants decreased and then increased, showing the minimum at a certain potential level. The latter indicated that the channel was released from the blocking by excessive hyperpolarization.4. The opening rate constant increased in spite of the fixed concentration of the blocking cation (10 muM-Cs), when the external K concentration was raised from 200 mM to 400 mM. This result suggested that there are interactions within the channel between the blocking cation and the K ion.5. When there were two kinds of blocking cations such as Na and Cs, the kinetic properties in a single channel indicated that the two kinds of blocking cations blocked the single channel independently.6. The single channel conductance of the anomalous K rectifier in 200 mM-Na-containing 200 mM-K solutions was about 1.5 times larger than that in Na-free 200 mM-K solutions.7. The single channel conductances in 100, 200 and 400 mM-K solution with 10 muM-Cs were 5.0, 7.1 and 12.3 pS respectively, being roughly proportional to the square root of the K concentration.8. The density of the anomalous K rectifier channel in the tunicate egg cell was 0.039/mum(2).9. The amplitude of the single channel current increased with the rise of temperature, the Q(10) being 1.5.

Characterization of the inward-rectifying potassium current in cat ventricular myocytes.

“…Changes seen in current magnitude when [Na+],, is changed have also been reported in tunicate egg cells (Ohmori, 1978(Ohmori, , 1980Fukushima, 1982). Although the mechanism is not understood, Ohmori (1980) suggested an Na + dependence for channel activation (as well as inactivation) because of the increase in apparent channel activity seen using fluctuation analysis.…”

“…Although the mechanism is not understood, Ohmori (1980) suggested an Na + dependence for channel activation (as well as inactivation) because of the increase in apparent channel activity seen using fluctuation analysis. Fukushima (1982), however, suggested that extracellular Na + may facilitate single-channel conductance. The mechanism behind the effects in isolated cat ventricular myocytes was not investigated here; however, there are several possible consequences associated with the reduction of [Na+]o, many of which could modulate or regulate the IK~ conductance.…”

“…In tunicate egg cells (Ohmori, 1978(Ohmori, , 1980Fukushima, 1982) and frog skeletal muscle (Standen and Stanfield, 1979), the inactivation of the inward-rectifying K + current is altered by removing Na + from the extracellular solution. To deternfine the importance of extracellular Na + to the inactivation of IK~, [Na+],, was replaced with TMA.…”

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

“…The probable existence of sites separate from the ion channel, at which ions bind to modulate single channel lifetime or conductance, complicates the interpretation of experiments in which changes in the external solution composition alter the amplitude of current relaxations produced by step changes of membrane potential. For example Na+ ions increase the single-channel conductance of the inward rectifier in tunicate egg cell membranes (Fukushima, 1982) but are not themselves permeant. Potassium ions increase the conductance of the inward rectifier in skeletal muscle (Hestrin, 1981;Leech & Stanfield, 1981) and Purkinje fibres (DiFrancesco, 1982) and are also permeable.…”

Induction of haemodynamic oscillations in the perfused rat liver by K+ channel blockers.

“…TEA, Cs+ and 4-AP are relatively non-specific and inhibit both delayed rectifying and Ca2+-activated K+ channels (Hille, 1984;Latorre, Oberhauser, Labarca & Alvarez, 1989 (Fukushima, 1982).…”