Effects of Density and Gating of Delayed-Rectifier Potassium Channels on Resting Membrane Potential and its Fluctuations

1996 ◽  
Vol 154 (3) ◽  
pp. 267-274 ◽  
Author(s):  
S. Marom ◽  
H. Salman ◽  
V. Lyakhov ◽  
E. Braun
Keyword(s):  
Membrane Potential ◽  
Potassium Channels ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Effects Of Density

Delayed rectifier potassium currents induced in activated rat microglia set the resting membrane potential

1998 ◽  
Vol 242 (2) ◽  
pp. 73-76 ◽  
Author(s):  
Sungkwon Chung ◽  
Eunhye Joe ◽  
Heun Soh ◽  
Moo-Yeol Lee ◽  
Hyo-Weon Bang
Keyword(s):  
Membrane Potential ◽  
Potassium Currents ◽  
Resting Membrane Potential ◽  
Delayed Rectifier

Local Anesthetic Inhibition of Baseline Potassium Channels with Two Pore Domains in Tandem 

1999 ◽  
Vol 90 (4) ◽  
pp. 1092-1102 ◽  
Author(s):  
Christoph H. Kindler ◽  
Spencer C. Yost ◽  
Andrew T. Gray
Keyword(s):  
Membrane Potential ◽  
Potassium Channels ◽  
Local Anesthetic ◽  
Local Anesthetics ◽  
Resting Membrane Potential ◽  
Electrode Voltage ◽  
Primary Amino ◽  
Anesthetic Action ◽  
Pore Domain ◽  
Pore Domains

Background Recently, a new structural family of potassium channels characterized by two pore domains in tandem within their primary amino acid sequence was identified. These tandem pore domain potassium channels are not gated by voltage and appear to be involved in the control of baseline membrane conductances. The goal of this study was to identify mechanisms of local anesthetic action on these channels. Methods Oocytes of Xenopus laevis were injected with cRNA from five cloned tandem pore domain baseline potassium channels (TASK, TREK-1, TOK1, ORK1, and TWIK-1), and the effects of several local anesthetics on the heterologously expressed channels were assayed using two-electrode voltage-clamp and current-clamp techniques. Results Bupivacaine (1 mM) inhibited all studied tandem pore potassium channels, with TASK inhibited most potently. The potency of inhibition was directly correlated with the octanol: buffer distribution coefficient of the local anesthetic, with the exception of tetracaine, to which TASK is relatively insensitive. The approximate 50% inhibitory concentrations of TASK were 709 microM mepivacaine, 222 microM lidocaine, 51 microM R(+)-ropivacaine, 53 microM S(-)-ropivacaine, 668 microM tetracaine, 41 microM bupivacaine, and 39 microM etidocaine. Local anesthetics (1 mM) significantly depolarized the resting membrane potential of TASK cRNA-injected oocytes compared with saline-injected control oocytes (tetracaine 22+/-6 mV rs. 7+/-1 mV, respectively, and bupivacaine 31+/-7 mV vs. 6+/-4 mV). Conclusions Local anesthetics inhibit tandem pore domain baseline potassium channels, and they could depolarize the resting membrane potential of cells expressing these channels. Whether inhibition of these channels contributes to conduction blockade or to the adverse effects of local anesthetics remains to be determined.

A function of delayed rectifier potassium channels in glial cells: maintenance of an auxiliary membrane potential under pathological conditions

2000 ◽  
Vol 862 (1-2) ◽  
pp. 187-193 ◽  
Author(s):  
Thomas Pannicke ◽  
Frank Faude ◽  
Andreas Reichenbach ◽  
Winfried Reichelt
Keyword(s):  
Membrane Potential ◽  
Potassium Channels ◽  
Glial Cells ◽  
Delayed Rectifier ◽  
Pathological Conditions

Tamoxifen inhibits Na+ and K+ currents in rat ventricular myocytes

2003 ◽  
Vol 285 (2) ◽  
pp. H661-H668 ◽  
Author(s):  
Jianying He ◽  
Margaret E. Kargacin ◽  
Gary J. Kargacin ◽  
Christopher A. Ward
Keyword(s):  
Membrane Potential ◽  
Ventricular Myocytes ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Rat Ventricular Myocytes ◽  
Life Threatening ◽  
Prolonged Qt Interval ◽  
Electrophysiological Mechanism ◽  
K Currents ◽  
Arrhythmogenic Effects

Tamoxifen is an estrogen receptor antagonist used in the treatment of breast cancer. However, tamoxifen has been shown to induce QT prolongation of the electrocardiogram, thereby potentially causing life-threatening polymorphic ventricular arrhythmias. The purpose of the present study was to elucidate the electrophysiological mechanism(s) that underlie the arrhythmogenic effects of tamoxifen. We used standard ruptured whole cell and perforated patch-clamping techniques on rat ventricular myocytes to investigate the effects of tamoxifen on cardiac action potential (AP) waveforms and the underlying K+ currents. Tamoxifen (3 μmol/l) markedly prolonged AP duration, decreased maximal rate of depolarization, and decreased resting membrane potential. At this concentration, tamoxifen significantly depressed the Ca2+-independent transient outward K+ current ( Ito), sustained outward delayed rectifier K+ current ( Isus), inward rectifier K+ current ( IK1), and Na+ current ( INa) in the myocytes. Lower concentrations of tamoxifen (1 μmol/l) also decreased the resting membrane potential and significantly depressed IK1 to 79 ± 5% ( n = 5; at –120 mV) of pretreatment values. The results of this study indicate that inhibition of Ito, Isus, and IK1 by tamoxifen may underlie AP prolongation in cardiac myocytes and thereby contribute to prolonged QT interval observed in patients.

scholarly journals A Ba2+-Sensitive K+ Current Contributes to the Resting Membrane Potential of Neurons in Rat Suprachiasmatic Nucleus

2002 ◽  
Vol 88 (2) ◽  
pp. 869-878 ◽  
Author(s):  
Marcel de Jeu ◽  
Alwin Geurtsen ◽  
Cyriel Pennartz
Keyword(s):  
Membrane Potential ◽  
Suprachiasmatic Nucleus ◽  
Voltage Dependence ◽  
Brain Slices ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
M Current ◽  
Whole Cell Patch Clamp

A Ba2+-sensitive K+ current was studied in neurons of the suprachiasmatic nucleus (SCN) using the whole cell patch-clamp technique in acutely prepared brain slices. This Ba2+-sensitive K+ current was found in approximately 90% of the SCN neurons and was uniformly distributed across the SCN. Current-clamp studies revealed that Ba2+ (500 μM) reversibly depolarized the membrane potential by 6.7 ± 1.3 mV ( n = 22) and concomitantly Ba2+ induced an increase in the spontaneous firing rate of 0.8 ± 0.2 Hz ( n = 12). The Ba2+-evoked depolarizations did not depend on firing activity or spike dependent synaptic transmission. No significant day/night difference in the hyperpolarizing contribution to the resting membrane potential of the present Ba2+-sensitive current was observed. Voltage-clamp experiments showed that Ba2+ (500 μM) reduced a fast-activating, voltage-dependent K+ current. This current was activated at levels below firing threshold and exhibited outward rectification. The Ba2+-sensitive K+ current was strongly reduced by tetraethylammonium (TEA; 20 and 60 mM) but was insensitive to 4-aminopyridine (4-AP; 5 mM) and quinine (100 μM). A component of Ba2+-sensitive K+ current remaining in the presence of TEA exhibited no clear voltage dependence and is less likely to contribute to the resting membrane potential. The voltage dependence, kinetics and pharmacological properties of the Ba2+- and TEA-sensitive K+ current make it unlikely that this current is a delayed rectifier, Ca2+-activated K+ current, ATP-sensitive K+ current, M-current or K+ inward rectifier. Our data are consistent with the Ba2+- and TEA-sensitive K+ current in SCN neurons being an outward rectifying K+ current of a novel identity or belonging to a known family of K+ channels with related properties. Regardless of its precise molecular identity, the current appears to exert a significant hyperpolarizing effect on the resting potential of SCN neurons.

Electrophysiological response of rat ventricular myocytes to acidosis

2002 ◽  
Vol 283 (1) ◽  
pp. H412-H422 ◽  
Author(s):  
Kimiaki Komukai ◽  
Fabien Brette ◽  
Caroline Pascarel ◽  
Clive H. Orchard
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Resting Potential ◽  
Disulfonic Acid ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Electrophysiological Response ◽  
Inwardly Rectifying

The effects of acidosis on the action potential, resting potential, L-type Ca2+( I Ca), inward rectifier potassium ( I K1), delayed rectifier potassium ( I K), steady-state ( I SS), and inwardly rectifying chloride ( I Cl,ir) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I Ca, I K1, and I SS were not significantly different in Epi and Endo cells, but I K was larger in Epi cells. Acidosis did not alter I Ca, I K1, or I K but decreased I SS; this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I SS underlies the prolongation of the action potential. I Cl,ir at control pH was Cd2+ sensitive but 4,4′-disothiocyanato-stilbene-2,2′-disulfonic acid resistant. Acidosis increased I Cl,ir; it is suggested that the acidosis-induced increase in I Cl,ir underlies the depolarization of the resting membrane potential.

Hyperglycemia induces mechanical hyperalgesia and depolarization of the resting membrane potential of primary nociceptive neurons: Role of ATP-sensitive potassium channels

2019 ◽  
Vol 401 ◽  
pp. 55-61 ◽  
Author(s):  
Taís de Campos Lima ◽  
Débora de Oliveira Santos ◽  
Júlia Borges Paes Lemes ◽  
Luana Mota Chiovato ◽  
Celina Monteiro da Cruz Lotufo
Keyword(s):  
Membrane Potential ◽  
Potassium Channels ◽  
Mechanical Hyperalgesia ◽  
Resting Membrane Potential ◽  
Nociceptive Neurons
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