Tetraethylammonium blockade of calcium-activated potassium channels in clonal anterior pituitary cells

Wong, Brendan S.; Adler, Michaël

doi:10.1007/bf00585303

Cited by 44 publications

(17 citation statements)

References 31 publications

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“…Voltage-dependent Ca 2+ currents were insignificant at the external Ca 2+ concentration of 0.2 mM. The minimal concentration of TEA used was 1 mM, which inhibited the Ca 2+ -activated K + currents and the fast I DR (Wong and Adler, 1986). The calculated I A τ inact was not affected by the holding potential.…”

Section: Methodsmentioning

confidence: 88%

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Alvado

Allen

2008

Brain Research

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Identifying the mechanisms that drive suprachiasmatic nucleus (SCN) neurons to fire action potentials with a higher frequency during the day than during the night is an important goal of circadian neurobiology. Selective chemical tools with defined mechanisms of action on specific ion channels are required for successful completion of these studies. The transient K + current (I A ) plays an active role in neuronal action potential firing and may contribute to modulating the circadian firing frequency. Tetraethylammonium (TEA) is frequently used to inhibit delayed rectifier K + currents (I DR ) during electrophysiological recordings of I A . Depolarizing voltage-clamped hamster SCN neurons from a hyperpolarized holding potential activated both I A and I DR . Holding the membrane potential at depolarized values inactivated I A and only the I DR was activated during a voltage step. The identity of I A was confirmed by applying 4-aminopyridine (5 mM), which significantly inhibited I A . Reducing the TEA concentration from 40 mM to 1 mM significantly decreased the I A inactivation time constant (τ inact ) from 9.8 ± 3.0 ms to 4.9 ± 1.2 ms. The changes in I A τ inact were unlikely to be due to a surface charge effect. The I A amplitude was not affected by TEA at any concentration or membrane potential. The isosmotic replacement of NaCl with choline chloride had no effect in I A kinetics demonstrating that the TEA effects were not due to a reduction of extracellular NaCl. We conclude that TEA modulates, in a concentration dependent manner, τ inact but not I A amplitude in hamster SCN neurons. SectionNeurophysiology; Neuropharmacology and other forms of Intercellular Communication

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Section: Methodsmentioning

confidence: 88%

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Alvado

Allen

2008

Brain Research

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“…delayed rectifiers; 0.3 (Dubois, 1981) to >200 mM (Tasaki & Hagiwara, 1957); calcium-activated K 0.14 (Bokvist et al, 1990) to 52.2 mM (Wong & Adler, 1986); inward rectifiers, <10 mM (Schachtman et al, 1992)]. here to have a high Kd for external TEA block (-50 mM).…”

Section: Tetraethylammoniummentioning

confidence: 93%

Pharmacology of stretch‐activated K channels in Lymnaea neurones

Small

Morris

1995

British J Pharmacology

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1 Single-channel recording was used to describe the pharmacology of stretch-activated K channels in Lymnaea neurones using channel blockers amiloride, tetraethylammonium (TEA), quinidine, gadolinium (Gd) and diltiazem. 2 Amiloride, TEA and quinidine applied to the outside face of the membrane all produced a fast flickery block of stretch-activated K channels. All of these agents were without effect when applied at the inside face at concentrations as high as 10, 200 and 10 mM respectively. Neither Gd nor diltiazem had any effect on stretch-activated K channels extracellularly (100 JiM).3 Amiloride, TEA and quinidine block were voltage-independent with IC,0 values at positive (and negative membrane potentials of 2.3 (and 2.0) mM, 48 (and 54) mM and 0.8 (and 0.7) mM respectively. Woodhull plots for TEA and quinidine block confirmed the voltage independence of stretch-activated K channel block by these agents.4 Hill plots of the amilorde, TEA and quinidine block yield Hill coefficients at positive (and negative) membrane potentials of 1.7 (and 1.5), 1.4 (and 1.2) and 1.5 (and 1.6 mM) respectively. 5 Ethanol (3%) had no apparent effect on stretch-activated K channel kinetics or conductance yet reduced the efficacy of quinidine block. 6 The above pharmacological fingerprint of the stretch-activated K channel is discussed with reference to other K-selective and stretch-activated channels.

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“…The Ca 21 -influx/Cl 2 -efflux/ K 1 -efflux sequence in signal generation may explain the depolarizing direction, but different fluxes are needed to explain signals of the negative sign, such as K 1 -efflux preceding Cl 2 -efflux. The latter was proved by blocking K 1 channels with 1 mM tetraethylammoniumchloride (TEA 1 ), acting on both sides of the membranes (Wong and Adler, 1986) and applied to the artificial pond water (APW) medium of the stem (Fig. 1).…”

Section: Long-distance Electrical Signalingmentioning

confidence: 99%

Characteristics of Electrical Signals in Poplar and Responses in Photosynthesis

et al. 2005

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To gain an understanding of the role of electrical signaling in trees, poplar (Populus trichocarpa, Populus tremula 3 P. tremuloides) shoots were stimulated by chilling as well as flaming. Two kinds of signal propagation were detected by microelectrode measurements (aphid technique) in the phloem of leaf veins: (1) basipetal, short-distance signaling that led to rapid membrane hyperpolarization caused by K 1 -efflux within the leaf lamina; and (2) acropetal, long-distance signaling that triggered depolarization of the membrane potential in the leaf phloem. In the latter, the depolarizing signals travel across the stem from the manipulated leaves to adjacent leaves where the net CO 2 uptake rate is temporarily depressed toward compensation. With regard to photosystem II, both heat-induced long-distance and short-distance signaling were investigated using two-dimensional ''imaging'' analysis of chlorophyll fluorescence. Both types of signaling significantly reduced the quantum yield of electron transport through photosystem II. Imaging analysis revealed that the signal that causes yield reduction spreads through the leaf lamina. Coldblocking of the stem proved that the electrical signal transmission via the phloem becomes disrupted, causing the leaf gas exchange to remain unaffected. Calcium-deficient trees showed a marked contrast inasmuch as the amplitude of the electrical signal was distinctly reduced, concomitant with the absence of a significant response in leaf gas exchange upon flame wounding. In summary, the above results led us to conclude that calcium as well as potassium is involved in the propagation of phloem-transmitted electrical signals that evoke specific responses in the photosynthesis of leaves.Electrical signaling in plants was first revealed in the 1870s in insectivorous plants by Burdon-Sanderson (1873) and Darwin (1875). In the 20th century, evidence for the existence of action potentials was presented in a broad array of plant species, irrespective of the presence of rapid leaf movements (Bose, 1924;Pickard, 1973). Most of the research on electrical signaling dealt with responses evoked by wounding of aboveground organs, providing insights into various processes of plant physiology. Molecular tools made it possible to detect rapid changes in gene expression (Davies and Schuster, 1981;Stankovic and Davies, 1997) as well as activation of proteinase inhibitor genes within plants (Bowles, 1990;Ryan, 1990;Wildon et al., 1992) upon wounding, even across long distances. Wildon et al. (1992) showed the chemical signals evoked by wounding in the phloem to be significantly slower than the rapid changes in membrane potential. Electrical signals that were generated and transmitted from distant plant parts arrived at responding tissues well before the initiation of transcript accumulation. Vian et al. (1999) induced rapid and systemic accumulation of chloroplast mRNA-binding protein transcripts, in tomato (Lycopersicon esculentum), after flame stimulus. In addition to translation and transcription, evid...

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Tetraethylammonium blockade of calcium-activated potassium channels in clonal anterior pituitary cells

Cited by 44 publications

References 31 publications

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Tetraethylammonium (TEA) increases the inactivation time constant of the transient K+ current in suprachiasmatic nucleus neurons

Pharmacology of stretch‐activated K channels in Lymnaea neurones

Characteristics of Electrical Signals in Poplar and Responses in Photosynthesis

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