ArticleBiophysical journal1997
Intracellular Ca2+ inactivates L-type Ca2+ channels with a Hill coefficient of approximately 1 and an inhibition constant of approximately 4 microM by reducing channel's open probability.
Article in Biophysical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 51 citations in OpenAlex.
- An electrophysiological and kinematic model of Paramecium, the "swimming neuron".PLoS computational biology · 2023Article
- Models of the cardiac L-type calcium current: A quantitative review.WIREs mechanisms of disease · 2023Review
- The Cav1.2 N terminus contains a CaM kinase site that modulates channel trafficking and function.Pflugers Archiv : European journal of physiology · 2015Article
- Data-based theoretical identification of subcellular calcium compartments and estimation of calcium dynamics in cardiac myocytes.The Journal of physiology · 2012Article
- Calpastatin domain L is a partial agonist of the calmodulin-binding site for channel activation in Cav1.2 Ca2+ channels.The Journal of biological chemistry · 2011Article
- Influence of pH on Ca²⁺ current and its control of electrical and Ca²⁺ signaling in ventricular myocytes.The Journal of general physiology · 2011Article
- Microdomain [Ca²⁺] near ryanodine receptors as reported by L-type Ca²⁺ and Na+/Ca²⁺ exchange currents.The Journal of physiology · 2011Article
- Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.Biophysical journal · 2007Article
- Nitric oxide inhibits capacitative Ca2+ entry by suppression of mitochondrial Ca2+ handling.British journal of pharmacology · 2002Article
- Molecular determinant for run-down of L-type Ca2+ channels localized in the carboxyl terminus of the 1C subunit.The Journal of physiology · 2000Article
- Regulation of ion channels in myocardial cells and protection of ischemic myocardium.Heart failure reviews · 2000Review
- Syntaxin 1 interacts with the L(D) subtype of voltage-gated Ca(2+) channels in pancreatic beta cells.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Ca2+-sensitive inactivation of L-type Ca2+ channels depends on multiple cytoplasmic amino acid sequences of the alpha1C subunit.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The patch-clamp technique was used to characterize the mechanism of Ca2+-induced inactivation of cardiac L-type Ca2+ channel alpha(1C-a) + beta3 subunits stably expressed in CHO cells. Single Ca2+ channel activity was monitored with 96 mM Ba2+ as charge carrier in the presence of 2.5 microM (-)BAYK 8644 and calpastatin plus ATP. This enabled stabilization of channel activity in the inside-out patch and allowed for application of steady-state Ca2+ concentrations to the intracellular face of excised membrane patches in an attempt to provoke Ca2+-induced inactivation. Inactivation was found to occur specifically with Ca2+ since it was not observed upon application of Ba2+. Ca2+-dependent inhibition of mean Ca2+ channel activity was characterized by a Hill coefficient close to 1. Ca2+ binding to open and closed states of the channel obtained during depolarization apparently occurred with similar affinity yielding half-maximal inhibition of Ca2+ channel activity at approximately 4 microM. This inhibition manifested predominantly in a reduction of the channel's open probability whereas availability remained almost unchanged. The reduction in open probability was achieved by an increase in first latencies and a decrease in channel opening frequency as well as channel open times. At high (12-28 microM) Ca2+ concentrations, 72% of inhibition occurred due to a stabilization of the closed state and the remaining 28% by a destabilization of the open state. Our results suggest that binding of one calcium ion to a regulatory domain induces a complex alteration in the kinetic properties of the Ca2+ channel and support the idea of a single EF hand motif as the relevant Ca2+ binding site on the alpha1 subunit.
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