ArticleThe Journal of general physiology1997
Ion-dependent inactivation of barium current through L-type calcium channels.
Article in The Journal of general physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
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- How CaThe Journal of general physiology · 2019Article
- Lead poisoning: acute exposure of the heart to lead ions promotes changes in cardiac function and Cav1.2 ion channels.Biophysical reviews · 2017Review
- Mechanisms of the cyclic nucleotide cross-talk signaling network in cardiac L-type calcium channel regulation.Journal of molecular and cellular cardiology · 2017Article
- The Rotavirus NSP4 Viroporin Domain is a Calcium-conducting Ion Channel.Scientific reports · 2017Article
- Potassium channels in the Cx43 gap junction perinexus modulate ephaptic coupling: an experimental and modeling study.Pflugers Archiv : European journal of physiology · 2016Article
- A human ventricular myocyte model with a refined representation of excitation-contraction coupling.Biophysical journal · 2015Article
- Impaired calcium-calmodulin-dependent inactivation of Cav1.2 contributes to loss of sarcoplasmic reticulum calcium release refractoriness in mice lacking calsequestrin 2.Journal of molecular and cellular cardiology · 2015Article
- Characterization of Cav1.4 complexes (α11.4, β2, and α2δ4) in HEK293T cells and in the retina.The Journal of biological chemistry · 2015Article
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Coordinated regulation of murine cardiomyocyte contractility by nanomolar (-)-epigallocatechin-3-gallate, the major green tea catechin.Molecular pharmacology · 2012Article
- Theoretical study of L-type Ca(2+) current inactivation kinetics during action potential repolarization and early afterdepolarizations.The Journal of physiology · 2012Article
- Influence of pH on Ca²⁺ current and its control of electrical and Ca²⁺ signaling in ventricular myocytes.The Journal of general physiology · 2011Article
- Simulation of the undiseased human cardiac ventricular action potential: model formulation and experimental validation.PLoS computational biology · 2011Article
- Interplay of voltage and Ca-dependent inactivation of L-type Ca current.Progress in biophysics and molecular biology · 2010Review
- Ca(2+)-dependent components of inactivation of unitary cardiac L-type Ca(2+) channels.The Journal of physiology · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
It is widely believed that Ba2+ currents carried through L-type Ca2+ channels inactivate by a voltage-dependent mechanism similar to that described for other voltage-dependent channels. Studying ionic and gating currents of rabbit cardiac Ca2+ channels expressed in different subunit combinations in tsA201 cells, we found a phase of Ba2+ current decay with characteristics of ion-dependent inactivation. Upon a long duration (20 s) depolarizing pulse, IBa decayed as the sum of two exponentials. The slow phase (tau approximately 6 s, 21 degrees C) was parallel to a reduction of gating charge mobile at positive voltages, which was determined in the same cells. The fast phase of current decay (tau approximately 600 ms), involving about 50% of total decay, was not accompanied by decrease of gating currents. Its amplitude depended on voltage with a characteristic U-shape, reflecting reduction of inactivation at positive voltages. When Na+ was used as the charge carrier, decay of ionic current followed a single exponential, of rate similar to that of the slow decay of Ba2+ current. The reduction of Ba2+ current during a depolarizing pulse was not due to changes in the concentration gradients driving ion movement, because Ba2+ entry during the pulse did not change the reversal potential for Ba2+. A simple model of Ca(2+) -dependent inactivation (Shirokov, R., R. Levis, N. Shirokova, and F., Ríos. 1993. J. Gen. Physiol. 102:1005-1030) robustly accounts for fast Ba2+ current decay assuming the affinity of the inactivation site on the alpha 1 subunit to be 100 times lower for Ba2+ than Ca2+.
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