Strong voltage-dependent inward rectification of inward rectifier K+ channels is caused by intracellular spermine

@article{Fakler1995StrongVI,
  title={Strong voltage-dependent inward rectification of inward rectifier K+ channels is caused by intracellular spermine},
  author={Bernd Fakler and Uwe Brändle and Elisabeth Glowatzki and Susanne Weidemann and Hans Peter Zenner and Johann Peter Ruppersberg},
  journal={Cell},
  year={1995},
  volume={80},
  pages={149-154}
}
Inward rectifier K+ channels mediate the K+ conductance at resting potential in many types of cell. Since these K+ channels do not pass outward currents (inward rectification) when the cell membrane is depolarized beyond a trigger threshold, they play an important role in controlling excitability. Both a highly voltage-dependent block by intracellular Mg2+ and an endogenous gating process are presently assumed to underly inward rectification. It is shown that strong voltage dependence of… Expand
Mechanism of rectification in inward-rectifier K+ channels.
  • Zhe Lu
  • Chemistry, Medicine
  • Annual review of physiology
  • 2004
Inward rectifiers are a class of K+ channels that can conduct much larger inward currents at membrane voltages negative to the K+ equilibrium potential than outward currents at voltages positive toExpand
Polyamines as gating molecules of inward-rectifier K+ channels.
TLDR
The present molecular-biophysical understanding of inward-rectification and its physiological consequences is the topic of this review. Expand
Pore Block versus Intrinsic Gating in the Mechanism of Inward Rectification in Strongly Rectifying Irk1 Channels
TLDR
It is found that residual rectification is caused primarily by the commonly used pH buffer HEPES and/or some accompanying impurity, and inward rectification in the strong rectifier IRK1, as in the weak rectifier ROMK1 can be accounted for by voltage-dependent block of its ion conduction pore by intracellular cations. Expand
Novel Gating Mechanism of Polyamine Block in the Strong Inward Rectifier K Channel Kir2.1
TLDR
Evidence is presented that high affinity polyamine block is not consistent with direct open channel block, but instead involves polyamines binding to another region of the channel (intrinsic gate) to form a blocking complex that occludes the pore. Expand
Time-dependent Outward Currents through the Inward Rectifier Potassium Channel IRK1
  • K. Ishihara
  • Chemistry, Medicine
  • The Journal of general physiology
  • 1997
TLDR
It is indicated that blockage of IRK1 by molecules with distinct affinities, spermine and Mg2+ (putrescine), elicits a transient increase in the outward IRK 1, which may contribute to repolarization of the cardiac action potential. Expand
IRK1 Inward Rectifier K+ Channels Exhibit No Intrinsic Rectification
TLDR
The study helps define the optimal experimental conditions for studying IRK1 and finds that both current relaxations can be accounted for by impurities in some common constituents of recording solutions, such as residual hydroxyethylpiperazine in HEPES and ethylenediamine in EDTA. Expand
Spermine Block of the Strong Inward Rectifier Potassium Channel Kir2.1
TLDR
A quantitative model incorporating both features showed excellent agreement with the steady-state and kinetic data, and accounts for previously described substate behavior induced by a variety of Kir2.1 channel blockers. Expand
Mg2+-dependent Gating and Strong Inward Rectification of the Cation Channel TRPV6
TLDR
The effects of intracellular Mg2+ on TRpV6 are partially reminiscent of the gating mechanism of inwardly rectifying K+ channels and may represent a novel regulatory mechanism for TRPV6 function in vivo. Expand
Magnesium‐independent activation of inward‐rectifying K+ channels in Vicia faba guard cells
TLDR
In guard cells, when cytosolic Mg2+ was either 3 mM or < I μM, activation times, deactivation times and the steady‐state voltage‐dependence of K+ channels remained unchanged. Expand
Classical Inward Rectifying Potassium Channels: Mechanisms of Inward Rectification
Potassium channels are highly selective for potassium ions over other cations. They have been broadly classified into two main families (Hille 1992). So-called “voltage-gated” K channels areExpand
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References

SHOWING 1-10 OF 42 REFERENCES
Electrostatic tuning of Mg2+ affinity in an inward-rectifier K+ channel
TLDR
It is shown that mutations at one position in the second transmembrane segment can alter the Mg2+affinity and convert a weakly rectifying channel (ROMK1) into a strong rectifier. Expand
The Mg2+ block and intrinsic gating underlying inward rectification of the K+ current in guinea‐pig cardiac myocytes.
TLDR
The blockade by Mg2+ and intrinsic gating of the channel, which underlie the rectification of the inward rectifier K+ current, was investigated using the oil‐gap voltage clamp method in isolated guinea‐pig ventricular cells and it is concluded that the instantaneous inward rectification on depolarization is due to the M g2+ block at physiological [Mg2-]i. Expand
Inward rectification of a potassium channel in cardiac ventricular cells depends on internal magnesium ions.
  • C. Vandenberg
  • Chemistry, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1987
TLDR
The mechanism of rectification of the inwardly rectifying potassium channel was examined with single-channel recording techniques in isolated ventricular myocytes from adult guinea pig heart to suggest that rectification is due to internal block by Mg2+, possibly the result of rapid block of the open channel. Expand
Specification of pore properties by the carboxyl terminus of inwardly rectifying K+ channels.
TLDR
The carboxyl terminus appears to have a major role in specifying the pore properties of IRKs, which maintain the resting membrane potential of cells and permit prolonged depolarization, such as during the cardiac action potential. Expand
Inward rectification in frog skeletal muscle fibres and its dependence on membrane potential and external potassium.
TLDR
Under hyperpolarization, K currents increased with time, but instantaneous current‐voltage relations also showed inward rectification, and the relationship between gK, the potassium chord conductance, and membrane potential depended on membrane potential and[K]o, but not on [K]i. Expand
Kir2.1 inward rectifier K+ channels are regulated independently by protein kinases and ATP hydrolysis
TLDR
Second messenger regulation of IRK1 (Kir2.1) inward rectifier K+ channels was investigated in giant inside-out patches from Xenopus oocytes and currents could be down-regulated by N-heptyl-5-chloro-1-naphthalenesulfonamide, a specific stimulator of protein kinase C (PKC), suggesting that PKA and PKC mediate inverse effects on Kir 2.1 channels. Expand
Intrinsic gating of inward rectifier in bovine pulmonary artery endothelial cells in the presence or absence of internal Mg2+
TLDR
Inward rectifier (IR) currents in bovine pulmonary artery endothelial cells have an intrinsic gating mechanism that is not due to Mg block, and the voltage dependence of alpha and beta shifted along with EK, as is characteristic of IR channels in other cells. Expand
Effects of external and internal K+ ions on magnesium block of inwardly rectifying K+ channels in guinea‐pig heart cells.
  • H. Matsuda
  • Chemistry, Medicine
  • The Journal of physiology
  • 1991
TLDR
Block of the inwardly rectifying K+ channel by intracellular Mg2+ was studied in guinea‐pig ventricular cells at varying external or internal K+ concentrations and blocking and unblocking rates were calculated on the assumption that the channel is composed of three identical conducting units and each unit is blocked by M g2+ independently. Expand
Voltage‐dependent activation of the inward‐rectifier potassium channel in the ventricular cell membrane of guinea‐pig heart.
  • Y. Kurachi
  • Chemistry, Medicine
  • The Journal of physiology
  • 1985
TLDR
The activation kinetics of the inward‐rectifier K+ channel were studied by single‐channel recording in isolated single cells of the guinea‐pig ventricle with two different extracellular concentrations of K+ and the noise analysis of the steady‐state current fluctuations revealed that the activation gate of the channel follows first‐order kinetics between the open and closed states. Expand
Cloned neuronal Ik(A) channels reopen during recovery from inactivation
TLDR
Although the current in response to the depolarization is rapidly inactivating, the current elicited by repolarization declines slowly and produces long-lasting afterhyperpolarizations under current-clamp conditions, implying an additional physiological role for Ik(A) channels, particularly those that activate positive to the threshold of excitation. Expand
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