scholarly journals KV2.1 K+ Channels Underlie Major Voltage-Gated K+ Outward Current in H9c2 Myoblasts.

2002 ◽  
Vol 52 (6) ◽  
pp. 507-514 ◽  
Author(s):  
Wei Wang ◽  
Naoki Hino ◽  
Hiroshi Yamasaki ◽  
Takashi Aoki ◽  
Rikuo Ochi
Keyword(s):  
Outward Current ◽  
K Channels ◽  
Voltage Gated ◽  
H9c2 Myoblasts ◽  
K Outward Current

Transient outward current carried by inwardly rectifying K+ channels in guinea pig ventricular myocytes dialyzed with low-K+ solution

2004 ◽  
Vol 287 (5) ◽  
pp. C1396-C1403 ◽  
Author(s):  
Pavel Zhabyeyev ◽  
Tatsuya Asai ◽  
Sergey Missan ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Transient Outward Current ◽  
K Channels ◽  
Voltage Gated ◽  
Voltage Gated Channels ◽  
Inwardly Rectifying ◽  
Low K ◽  
External K

There have been periodic reports of nonclassic (4-aminopyridine insensitive) transient outward K+ current in guinea pig ventricular myocytes, with the most recent one describing a novel voltage-gated inwardly rectifying type. In the present study, we have investigated a transient outward current that overlaps inward Ca2+ current ( ICa,L) in myocytes dialyzed with 10 mM K+ solution and superfused with Tyrode’s solution. Although depolarizations from holding potential ( Vhp) −40 to 0 mV elicited relatively small inward ICa,L in these myocytes, removal of external K+ or addition of 0.2 mM Ba2+ more than doubled the amplitude of the current. The basis of the enhancement of ICa,L was the suppression of a large transient outward K+ current. Similar enhancement was observed when Vhp was moved to −80 mV and test depolarizations were preceded by short prepulses to −40 mV. Investigation of the time and voltage properties of the outward K+ transient indicated that it was inwardly rectifying and unlikely to be carried by voltage-gated channels. The outward transient was attenuated in myocytes dialyzed with high-Mg2+ solution, accelerated in myocytes dialyzed with 100 μM spermine solution, and abolished with time in myocytes dialyzed with ATP-free solution. These and other findings suggest that the outward transient is a component of classic “time-independent” inwardly rectifying K+ current.

scholarly journals Diverse K+ channels in primary human T lymphocytes.

1992 ◽  
Vol 99 (5) ◽  
pp. 771-793 ◽  
Author(s):  
S C Lee ◽  
D I Levy ◽  
C Deutsch
Keyword(s):  
T Lymphocytes ◽  
Outward Current ◽  
Cell Voltage ◽  
Whole Cell ◽  
K Channels ◽  
Voltage Gated ◽  
T Lymphocyte Proliferation ◽  
Cell Recording ◽  
Gated Channel ◽  
K Current

We used patch clamp techniques to identify and characterize a variety of K+ channels in primary human peripheral T lymphocytes. The most common channel observed in cell-attached configuration was voltage gated and inactivating. In ensemble averages, the kinetics of its activation and inactivation were similar to those of the whole-cell, voltage-gated K+ current described previously (Cahalan, M. D., K. G. Chandy, T. E. DeCoursey, and S. Gupta. 1985. J. Physiol. [Lond.]. 358:197-237; Deutsch, C., D. Krause, and S. C. Lee. 1986. J. Physiol. [Lond.]. 372:405-423), suggesting that this channel underlies the major portion of the outward current in lymphocytes. A small fraction of the time, this or another very similar channel was observed to inactivate significantly more slowly. Another channel type observed in cell-attached recording was seen less frequently and was transient in its appearance. This channel has a unitary conductance of approximately 10 pS, similar to the voltage-gated channel, but its voltage-independent gating, lack of inactivation, and different kinetic parameters showed it to be distinct. In whole-cell recording there is often a significant plateau current during sustained depolarization. Experiments using whole-cell and excised outside-out configurations indicate that at least part of this residual current is carried by K+ and, as opposed to the predominant voltage-gated current, is charybdotoxin insensitive. These findings are consistent with evidence that implicates charybdotoxin-sensitive and -insensitive components in T lymphocyte proliferation and volume regulation.

scholarly journals Regulation of voltage-gated K+channels by glucose metabolism in pancreatic β-cells

FEBS Letters ◽  
2009 ◽  
Vol 583 (13) ◽  
pp. 2225-2230 ◽  
Author(s):  
Masashi Yoshida ◽  
Katsuya Dezaki ◽  
Shiho Yamato ◽  
Atsushi Aoki ◽  
Hitoshi Sugawara ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
K Channels ◽  
Voltage Gated

scholarly journals The Antibacterial Activity of Human Neutrophils and Eosinophils Requires Proton Channels but Not BK Channels

2006 ◽  
Vol 127 (6) ◽  
pp. 659-672 ◽  
Author(s):  
Jon K. Femling ◽  
Vladimir V. Cherny ◽  
Deri Morgan ◽  
Balázs Rada ◽  
A. Paige Davis ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Respiratory Burst ◽  
Essential Role ◽  
Outward Current ◽  
Bk Channels ◽  
Bk Channel ◽  
Human Neutrophils ◽  
H2o2 Production ◽  
Proton Channels ◽  
Voltage Gated

Electrophysiological events are of central importance during the phagocyte respiratory burst, because NADPH oxidase is electrogenic and voltage sensitive. We investigated the recent suggestion that large-conductance, calcium-activated K+ (BK) channels, rather than proton channels, play an essential role in innate immunity (Ahluwalia, J., A. Tinker, L.H. Clapp, M.R. Duchen, A.Y. Abramov, S. Page, M. Nobles, and A.W. Segal. 2004. Nature. 427:853–858). In PMA-stimulated human neutrophils or eosinophils, we did not detect BK currents, and neither of the BK channel inhibitors iberiotoxin or paxilline nor DPI inhibited any component of outward current. BK inhibitors did not inhibit the killing of bacteria, nor did they affect NADPH oxidase-dependent degradation of bacterial phospholipids by extracellular gIIA-PLA2 or the production of superoxide anion (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2^{.}}^{{-}}\) \end{document}). Moreover, an antibody against the BK channel did not detect immunoreactive protein in human neutrophils. A required role for voltage-gated proton channels is demonstrated by Zn2+ inhibition of NADPH oxidase activity assessed by H2O2 production, thus validating previous studies showing that Zn2+ inhibited \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{O}_{2^{.}}^{{-}}\) \end{document} production when assessed by cytochrome c reduction. In conclusion, BK channels were not detected in human neutrophils or eosinophils, and BK inhibitors did not impair antimicrobial activity. In contrast, we present additional evidence that voltage-gated proton channels serve the essential role of charge compensation during the respiratory burst.

scholarly journals Resin-acid derivatives as potent electrostatic openers of voltage-gated K channels and suppressors of neuronal excitability

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Nina E Ottosson ◽  
Xiongyu Wu ◽  
Andreas Nolting ◽  
Urban Karlsson ◽  
Per-Eric Lund ◽  
...  
Keyword(s):  
Neuronal Excitability ◽  
Resin Acid ◽  
K Channels ◽  
Voltage Gated

Voltage-Dependent Properties of Dendrites That Eliminate Location-Dependent Variability of Synaptic Input

1999 ◽  
Vol 81 (2) ◽  
pp. 535-543 ◽  
Author(s):  
Erik P. Cook ◽  
Daniel Johnston
Keyword(s):  
Synaptic Input ◽  
Outward Current ◽  
Compartment Model ◽  
Inward Current ◽  
Voltage Gated ◽  
Cable Properties ◽  
Dendritic Membrane ◽  
Voltage Dependent ◽  
Dendritic Location ◽  
Voltage Gated Channels

Voltage-dependent properties of dendrites that eliminate location-dependent variability of synaptic input. We examined the hypothesis that voltage-dependent properties of dendrites allow for the accurate transfer of synaptic information to the soma independent of synapse location. This hypothesis is motivated by experimental evidence that dendrites contain a complex array of voltage-gated channels. How these channels affect synaptic integration is unknown. One hypothesized role for dendritic voltage-gated channels is to counteract passive cable properties, rendering all synapses electrotonically equidistant from the soma. With dendrites modeled as passive cables, the effect a synapse exerts at the soma depends on dendritic location (referred to as location-dependent variability of the synaptic input). In this theoretical study we used a simplified three-compartment model of a neuron to determine the dendritic voltage-dependent properties required for accurate transfer of synaptic information to the soma independent of synapse location. A dendrite that eliminates location-dependent variability requires three components: 1) a steady-state, voltage-dependent inward current that together with the passive leak current provides a net outward current and a zero slope conductance at depolarized potentials, 2) a fast, transient, inward current that compensates for dendritic membrane capacitance, and 3) both αamino-3-hydroxy-5-methyl-4-isoxazolepropionic acid– and N-methyl-d-aspartate–like synaptic conductances that together permit synapses to behave as ideal current sources. These components are consistent with the known properties of dendrites. In addition, these results indicate that a dendrite designed to eliminate location-dependent variability also actively back-propagates somatic action potentials.

scholarly journals Voltage‐gated K+ Channels as Potential Therapeutic Targets for Lung Adenocarcinoma Therapy

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
SO YEONG LEE ◽  
SOO HWA JANG ◽  
SUN YOUNG CHOI ◽  
PAN DONG RYU
Keyword(s):  
Lung Adenocarcinoma ◽  
Therapeutic Targets ◽  
K Channels ◽  
Voltage Gated
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