Sarcoplasmic Reticulum K+ Channels from Human and Sheep Atrial Cells Display a Specific Electro-pharmacological Profile

Picard, L; Côté, Karel; Teijeira, J; Greentree, David; Rousseau, Éric

doi:10.1006/jmcc.2002.2041

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…Previous reports suggest that SR K + channels exhibit a single sub-conductance state of approximately 60–70 % of the fully open state. This sub-state has often been described as messy or noisy and there are quite wide variations in the reported amplitudes of the sub-conductance state [6, 10, 15, 19, 22, 26, 27]. We suggest that the noisy gating of this reported 60–70 % sub-conductance state actually reflects the rapid transitions between multiple sub-conductance states of the TRIC channels (see Figs.…”

Section: Discussionmentioning

confidence: 77%

TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model

Venturi

Matyjaszkiewicz

Pitt

et al. 2013

Pflugers Arch - Eur J Physiol

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Sarcoplasmic/endoplasmic reticulum (SR) and nuclear membranes contain two related cation channels named TRIC-A and TRIC-B. In many tissues, both subtypes are co-expressed, making it impossible to distinguish the distinct single-channel properties of each subtype. We therefore incorporated skeletal muscle SR vesicles derived from Tric-a-knockout mice into bilayers in order to characterise the biophysical properties of native TRIC-B without possible misclassification of the channels as TRIC-A, and without potential distortion of functional properties by detergent purification protocols. The native TRIC-B channels were ideally selective for cations. In symmetrical 210 mM K+, the maximum (full) open channel level (199 pS) was equivalent to that observed when wild-type SR vesicles were incorporated into bilayers. Analysis of TRIC-B gating revealed complex and variable behaviour. Four main sub-conductance levels were observed at approximately 80 % (161 pS), 60 % (123 pS), 46 % (93 pS), and 30 % (60 pS) of the full open state. Seventy-five percent of the channels were voltage sensitive with Po being markedly reduced at negative holding potentials. The frequent, rapid transitions between TRIC-B sub-conductance states prevented development of reliable gating models using conventional single-channel analysis. Instead, we used mean-variance plots to highlight key features of TRIC-B gating in a more accurate and visually useful manner. Our study provides the first biophysical characterisation of native TRIC-B channels and indicates that this channel would be suited to provide counter current in response to Ca2+ release from the SR. Further experiments are required to distinguish the distinct functional properties of TRIC-A and TRIC-B and understand their individual but complementary physiological roles.Electronic supplementary materialThe online version of this article (doi:10.1007/s00424-013-1251-y) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 77%

TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model

Venturi

Matyjaszkiewicz

Pitt

et al. 2013

Pflugers Arch - Eur J Physiol

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“…In 2008, we showed that RyRs conduct their own countercurrent (4). Before that, the needed countercurrent was generally believed to be mediated by the SR K þ channel (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Sarcoplasmic Reticulum K+ (TRIC) Channel Does Not Carry Essential Countercurrent during Ca2+ Release

Guo

Nani

Shonts

et al. 2013

Biophysical Journal

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The charge translocation associated with sarcoplasmic reticulum (SR) Ca(2+) efflux is compensated for by a simultaneous SR K(+) influx. This influx is essential because, with no countercurrent, the SR membrane potential (Vm) would quickly (<1 ms) reach the Ca(2+) equilibrium potential and SR Ca(2+) release would cease. The SR K(+) trimeric intracellular cation (TRIC) channel has been proposed to carry the essential countercurrent. However, the ryanodine receptor (RyR) itself also carries a substantial K(+) countercurrent during release. To better define the physiological role of the SR K(+) channel, we compared SR Ca(2+) transport in saponin-permeabilized cardiomyocytes before and after limiting SR K(+) channel function. Specifically, we reduced SR K(+) channel conduction 35 and 88% by replacing cytosolic K(+) for Na(+) or Cs(+) (respectively), changes that have little effect on RyR function. Calcium sparks, SR Ca(2+) reloading, and caffeine-evoked Ca(2+) release amplitude (and rate) were unaffected by these ionic changes. Our results show that countercurrent carried by SR K(+) (TRIC) channels is not required to support SR Ca(2+) release (or uptake). Because K(+) enters the SR through RyRs during release, the SR K(+) (TRIC) channel most likely is needed to restore trans-SR K(+) balance after RyRs close, assuring SR Vm stays near 0 mV.

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“…Ion channels with rather similar properties were described in the membranes of the sarcoplasmic reticulum [7]. The cited authors, however, were also unable to classify these channels as belonging to one well-known cationic channel type or another.…”

Section: Resultsmentioning

confidence: 96%

Properties of Large-Conductance Cationic Channels in the Neuronal Nuclear Envelope

2011

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The genetic apparatus of the nucleus of eukaryotic cells is surrounded by the nuclear envelope containing ion channels with different biophysical properties. The channels responsible for calcium release from the nuclear envelope into the intranuclear space have attracted special attention. As we found, a great number of large-conductance ion channels selective with respect to monovalent cations and impermeable for bivalent cations are present in all membranes where inositol trisphosphate receptors are expressed. We showed that channels of this type are insensitive to blockers of potassium channels and, according to their properties, cannot be attributed to one well-known type of ion channels or another. In addition, since their blockers remain unknown, these channels at present cannot be isolated and cloned. Channels of this type deserve further investigation; we hypothesize that large-conductance cationic channels can be involved in the control of the duration of Са 2+ release from the calcium store.

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Sarcoplasmic Reticulum K+ Channels from Human and Sheep Atrial Cells Display a Specific Electro-pharmacological Profile

Cited by 18 publications

References 38 publications

TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model

TRIC-B channels display labile gating: evidence from the TRIC-A knockout mouse model

Sarcoplasmic Reticulum K+ (TRIC) Channel Does Not Carry Essential Countercurrent during Ca2+ Release

Properties of Large-Conductance Cationic Channels in the Neuronal Nuclear Envelope

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