ArticleBiophysical journal2015
Interbeat interval modulation in the sinoatrial node as a result of membrane current stochasticity-a theoretical and numerical study.
Article in Biophysical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Cardiac Pacemaker Cells Harness Stochastic Resonance to Avoid Sinus Arrest.Circulation research · 2026Article
- Cardiac Pacemaker Cells Harness Stochastic Resonance to Ensure Fail-Safe Operation at Low Rates Bordering on Sinus Arrest.bioRxiv : the preprint server for biology · 2026Article
- Computational insights on drug effects on intrinsic stochasticity of mouse pacemaker cell activity.Biophysical journal · 2025Article
- Evaluating in-vivo spontaneous firing rate in the brain based on neuronal noise modeling.Communications biology · 2025Article
- Emergent activity, heterogeneity, and robustness in a calcium feedback model of the sinoatrial node.Biophysical journal · 2023Article
- A Biased Diffusion Approach to Sleep Dynamics Reveals Neuronal Characteristics.Biophysical journal · 2019Article
- Neuronal noise as an origin of sleep arousals and its role in sudden infant death syndrome.Science advances · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
A single isolated sinoatrial pacemaker cell presents intrinsic interbeat interval (IBI) variability that is believed to result from the stochastic characteristics of the opening and closing processes of membrane ion channels. To our knowledge, a novel mathematical framework was developed in this work to address the effect of current fluctuations on the IBIs of sinoatrial pacemaker cells. Using statistical modeling and employing the Fokker-Planck formalism, our mathematical analysis suggests that increased stochastic current fluctuation variance linearly increases the slope of phase-4 depolarization, hence the rate of activations. Single-cell and two-dimensional computerized numerical modeling of the sinoatrial node was conducted to validate the theoretical predictions using established ionic kinetics of the rabbit pacemaker and atrial cells. Our models also provide, to our knowledge, a novel complementary or alternative explanation to recent experimental observations showing a strong reduction in the mean IBI of Cx30 deficient mice in comparison to wild-types, not fully explicable by the effects of intercellular decoupling.
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