ArticleBiophysical journal1998
Slow inactivation in human cardiac sodium channels.
Article in Biophysical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 102 citations in OpenAlex.
- Article
- The chemistry of electrical signaling in sodium channels from bacteria and beyond.Cell chemical biology · 2024Review
- Structural mechanism of voltage-gated sodium channel slow inactivation.Nature communications · 2024Article
- Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors.The Journal of general physiology · 2023Article
- High-throughput combined voltage-clamp/current-clamp analysis of freshly isolated neurons.Cell reports methods · 2023Article
- Inhibition of sodium conductance by cannabigerol contributes to a reduction of dorsal root ganglion neuron excitability.British journal of pharmacology · 2022Article
- Cannabidiol inhibits the skeletal muscle Nav1.4 by blocking its pore and by altering membrane elasticity.The Journal of general physiology · 2021Article
- Mechanisms and models of cardiac sodium channel inactivation.Channels (Austin, Tex.) · 2017Review
- Differential calcium sensitivity in NaThe Journal of physiology · 2017Article
- Dynamical Timescale Explains Marginal Stability in Excitability Dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Lacosamide Inhibition of Nav1.7 Voltage-Gated Sodium Channels: Slow Binding to Fast-Inactivated States.Molecular pharmacology · 2017Article
- A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2016Review
- Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants.The Journal of physiology · 2015Article
- Block of human cardiac sodium channels by lacosamide: evidence for slow drug binding along the activation pathway.Molecular pharmacology · 2014Article
- Small molecule cardiogenol C upregulates cardiac markers and induces cardiac functional properties in lineage-committed progenitor cells.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014Article
- DIFFERENCES IN IONIC CURRENTS BETWEEN CANINE MYOCARDIAL AND PURKINJE CELLS.Physiological reports · 2013Article
- Post-partum variation in the expression of paternal care is unrelated to urinary steroid metabolites in marmoset fathers.Hormones and behavior · 2013Article
- The role of a voltage-dependent Ca2+ channel intracellular linker: a structure-function analysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Extracellular proton modulation of the cardiac voltage-gated sodium channel, Nav1.5.Biophysical journal · 2011Article
- The outer vestibule of the Na+ channel-toxin receptor and modulator of permeation as well as gating.Marine drugs · 2010Review
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4 authors at 1 institution in 1 country.
Funding
Abstract
The available pool of sodium channels, and thus cell excitability, is regulated by both fast and slow inactivation. In cardiac tissue, the requirement for sustained firing of long-duration action potentials suggests that slow inactivation in cardiac sodium channels may differ from slow inactivation in skeletal muscle sodium channels. To test this hypothesis, we used the macropatch technique to characterize slow inactivation in human cardiac sodium channels heterologously expressed in Xenopus oocytes. Slow inactivation was isolated from fast inactivation kinetically (by selectively recovering channels from fast inactivation before measurement of slow inactivation) and structurally (by modification of fast inactivation by mutation of IFM1488QQQ). Time constants of slow inactivation in cardiac sodium channels were larger than previously reported for skeletal muscle sodium channels. In addition, steady-state slow inactivation was only 40% complete in cardiac sodium channels, compared to 80% in skeletal muscle channels. These results suggest that cardiac sodium channel slow inactivation is adapted for the sustained depolarizations found in normally functioning cardiac tissue. Complete slow inactivation in the fast inactivation modified IFM1488QQQ cardiac channel mutant suggests that this impairment of slow inactivation may result from an interaction between fast and slow inactivation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.