Potassium currents in frog ventricular muscle: evidence from voltage clamp currents and extracellular K accumulation.

Cleemann, Lars; Morad, Martin

doi:10.1113/jphysiol.1979.sp012609

Cited by 48 publications

(28 citation statements)

References 27 publications

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“…This type of explanation is not fundamentally different from the assumptions made in different models proposed to explain inward rectification (Standen & Stanfield, 1978;Ciani et al 1978;Cleeman & Morad, 1979;Hille & Schwarz, 1978). Inward rectification, according to these models, is due to the locking-in of a blocking particle on depolarization, and the unlocking on hyperpolarization; the removal of the block, requires the presence of extracellular K ions.…”

Section: Discussionmentioning

confidence: 86%

Induction and removal of inward‐going rectification in sheep cardiac Purkinje fibres

Carmeliet

1982

The Journal of Physiology

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SUMMARY1. In sheep cardiac Purkinje fibres superfused with K-free, Na-free medium, the membrane potential can be stable either at a low negative level (-50 mV) or at a high negative level (-100 mV). The mechanism underlying the existence of these two stable potential levels was investigated using the two-micro-electrode voltage-clamp technique.2. By applying a voltage clamp of a certain duration at an appropriate level the membrane potential could be shifted from one stable level to the other. The shift was observed in Cl-free medium, excluding a redistribution of Cl as a possible explanation.3. Currents during and following a voltage step and their change with amplitude and duration of the voltage step could not be explained on the basis of depletion or accumulation of K ions in the narrow extracellular clefts.4. Instantaneous currents determined from the high negative resting level showed a high conductance and a pronounced inward rectification, while measurements from the low negative resting level indicated a low conductance and absence of inward rectification. The steady-state current-voltage relation was dependent on the holding potential and showed memory or hysteresis.5. Estimation of the conductance by superimposed short voltage-clamp pulses showed an increase in conductance during a hyperpolarizing clamp from the low negative level and a decrease in conductance during a depolarizing clamp from the high negative level. The time-dependent current during a hyperpolarizing clamp from the low negative level reversed direction at a potential level corresponding to EK, assuming a cleft K concentration of about 1 mm. In the presence of 0-1 mM-Ba the time-dependent current was abolished.6. The results suggest that the shift between the two stable levels is due to a time-dependent conductance change in the K inward rectifier channel, iK1. The existence of memory excludes activation or de-activation only depending on the voltage gradient. Interaction of extracellular K ions with a site in the membrane is proposed as the activating mechanism.

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Section: Discussionmentioning

confidence: 86%

Induction and removal of inward‐going rectification in sheep cardiac Purkinje fibres

Carmeliet

1982

The Journal of Physiology

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“…Leak channels remain active at all potentials in contrast to inwardly rectifying cardiac potassium channels (49,50). Thus, Kcnk3 channels are expected to contribute not only to establishing resting membrane potential but to the height and length of action potentials and, therefore, the duration of myo- Single Kcnk3 channels were studied in outside-out patches with 100 mM potassium solution in the pipette.…”

Section: Discussionmentioning

confidence: 99%

Proton Block and Voltage Gating Are Potassium-dependent in the Cardiac Leak Channel Kcnk3

Lopes

Gallagher²,

Buck

et al. 2000

Journal of Biological Chemistry

153

179

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Potassium leak conductances were recently revealed to exist as independent molecular entities. Here, the genomic structure, cardiac localization, and biophysical properties of a murine example are considered. Kcnk3 subunits have two pore-forming P domains and unique functional attributes. At steady state, Kcnk3 channels behave like open, potassium-selective, transmembrane holes that are inhibited by physiological levels of proton. With voltage steps, Kcnk3 channels open and close in two phases, one appears to be immediate and one is time-dependent ( ‫؍‬ ϳ5 ms). Both proton block and gating are potassium-sensitive; this produces an anomalous increase in outward flux as external potassium levels rise because of decreased proton block. Single Kcnk3 channels open across the physiological voltage range; hence they are "leak" conductances; however, they open only briefly and rarely even after exposure to agents that activate other potassium channels.

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“…2 A- (33,34). K+ is thought to play a part in the activation of anomalous rectifier channels in addition to its role as charge carrier (6,34), and T1+ can substitute for K+ to activate the gating mechanism of the anomalously rectifying K+ channels in frog sartorius muscle (35) and starfish egg (34). In R15, the resting current observed when K+ is replaced by Tl+ is similar to that in controls and, in T1+ medium, serotonin evokes a current that must be both activated and conducted by lI (Fig.…”

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confidence: 99%

Serotonin increases an anomalously rectifying K+ current in the Aplysia neuron R15.

Benson¹,

Levitan²

1983

Proc. Natl. Acad. Sci. U.S.A.

107

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Previous work has shown that serotonin causes an increase in K+ conductance in the identified Aplysia neuron R15. This response is mediated by cAMP-dependent protein phosphorylation. The results presented here show that the K+ channel modulated by serotonin is an anomalous or inward rectifier (designated IR) that is present in R15 together with the three other distinct K+ channels previously described for this cell. Several lines of evidence indicate that this inward rectifier is partially activated in the resting cell and is further activated by serotonin. Voltage clamp analysis of resting and serotonin-evoked membrane currents at various external K+ concentrations shows that both currents have reversal potentials close to the potassium equilibrium potential, exhibit similar dependences in magnitude on external K+ concentration, and display marked anomalous rectification. The effects of particular monovalent and divalent cations are also similar on the resting and serotonin-evoked currents. RbV, Cs', and Ba24 block both currents while Tl can substitute for K+ as a charge carrier and channel activator in both. These properties are characteristic of anomalous rectifiers in other systems. Furthermore, measurement of the voltage dependence of inactivation for the fast transient K+ current shows that this current cannot account for the anomalously rectifying K+ conductance in R15. The inward rectifier is therefore a separate current mediated by its own channels, the activity of which can be modulated by serotonin.In 1949, Katz described a markedly nonlinear current-voltage relationship for the membranes of frog muscle fibers bathed in K4 medium (1). This ability to pass large inward but only small outward K4 currents has been called anomalous or inward rectification (2). Since then, anomalously rectifying K4 currents have been reported for a variety of muscle fibers (2-7) and for the egg cell membranes of tunicates (8) and starfish (9). However, in neuronal systems, anomalous rectification has been less precisely defined as an increase in membrane resistance with depolarization (10-13) and, in many cases, this resistance change is known to be due to the activation of an inward current carried by Ca24, Na+, or both (14,15 (25)(26)(27).As shown in Fig. 1, the resting conductance also decreases as the Ko decreases, suggesting that it is composed in part of * To whom reprint requests should be addressed. 3522The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S.C. §1734 solely to indicate this fact.

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Potassium currents in frog ventricular muscle: evidence from voltage clamp currents and extracellular K accumulation.

Cited by 48 publications

References 27 publications

Induction and removal of inward‐going rectification in sheep cardiac Purkinje fibres

Induction and removal of inward‐going rectification in sheep cardiac Purkinje fibres

Proton Block and Voltage Gating Are Potassium-dependent in the Cardiac Leak Channel Kcnk3

Serotonin increases an anomalously rectifying K+ current in the Aplysia neuron R15.

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