Nonlinear onset of calcium wave propagation in cardiac cells

Shiferaw, Yohannes

doi:10.1103/physreve.94.032405

Cited by 7 publications

(6 citation statements)

References 39 publications

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“…Indeed, we find that as the SR load builds, the system's response becomes aperiodic as triggered waves begin to disrupt synchronized Ca release in the cell. In fact, previous studies have demonstrated that a nonlinear dependence of Ca release on SR load leads to dynamical instabilities such as alternans and even chaos (25,(27)(28)(29)(30). In particular, we note the classic work of Díaz et al (31), who showed that when rat ventricular cells are paced periodically with small depolarizing pulses, Ca waves occur at alternate beats, causing an alternans response at the whole cell level.…”

Section: Discussionmentioning

confidence: 69%

Mechanism for Triggered Waves in Atrial Myocytes

Shiferaw

Aistrup

Wasserstrom

2017

Biophysical Journal

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Excitation-contraction coupling in atrial cells is mediated by calcium (Ca) signaling between L-type Ca channels and Ryanodine receptors that occurs mainly at the cell boundary. This unique architecture dictates essential aspects of Ca signaling under both normal and diseased conditions. In this study we apply laser scanning confocal microscopy, along with an experimentally based computational model, to understand the Ca cycling dynamics of an atrial cell subjected to rapid pacing. Our main finding is that when an atrial cell is paced under Ca overload conditions, Ca waves can then nucleate on the cell boundary and propagate to the cell interior. These propagating Ca waves are referred to as "triggered waves" because they are initiated by L-type Ca channel openings during the action potential. These excitations are distinct from spontaneous Ca waves originating from random fluctuations of Ryanodine receptor channels, and which occur after much longer waiting times. Furthermore, we argue that the onset of these triggered waves is a highly nonlinear function of the sarcoplasmic reticulum Ca load. This strong nonlinearity leads to aperiodic response of Ca at rapid pacing rates that is caused by the complex interplay between paced Ca release and triggered waves. We argue further that this feature of atrial cells leads to dynamic instabilities that may underlie atrial arrhythmias. These studies will serve as a starting point to explore the nonlinear dynamics of atrial cells and will yield insights into the trigger and maintenance of atrial fibrillation.

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Section: Discussionmentioning

confidence: 69%

Mechanism for Triggered Waves in Atrial Myocytes

Shiferaw

Aistrup

Wasserstrom

2017

Biophysical Journal

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“…This behavior resembles that of the sigmoid function model commonly used in stimulus-response models. [21,22] To further analyze this phenomenon, we employed the following sigmoid function to fit data points in Fig. 5:…”

Section: Data Analysis and Discussionmentioning

confidence: 99%

Characteristics of cell motility during cell collision

Ma 马,

Li 李,

Chen 陈

2024

Chinese Phys. B

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Quantitative examination of cellular motion and intercellullar interactions possesses substantial relevance for both biology and medicine. However, the effects of intercellular interactions during cellular locomotion remain under-explored in experimental research. As such, this study seeks to bridge this research gap, adopting Dictyostelium discoideum (Dicty) cells as a paradigm to investigate variations in cellular motion during reciprocal collisions. We aim to attain a comprehensive understanding of how cell interactions influence cell motion. By observing and processing the motion trajectories of colliding cells under diverse chemical environments, we calculated the diffusion coefficient (D) and the persistence time (τ), using mean square displacement. Our analysis of the relationship dynamics between D and τ prior to the collisions reveals intricate and non-monotonic alterations in cell movements during collisions. By quantitatively scrutinizing the τ trend, we were able to categorize the cellular responses to interactions under different conditions. Importantly, we ascertained that the effect of cell interactions during collisions in Dicty cells emulates a classical sigmoid function. This discovery suggests that cellular responses might comply with a pattern akin to the Weber-Fechner law.

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“…The effect of elevated [Na + ] i has been studied in computational models, finding calcium oscillations [60], that, depending on the model, appear via a supercritical Hopf [24] or a homoclinic bifurcation [25,26]. The instability of the diastolic resting state is thus well-known [61][62][63] and it plays an important role in the initiation of various cardiac arrhythmias [22]. However, the precise PLOS COMPUTATIONAL BIOLOGY mechanistic relationship between Ca and dangerous AP repolarization is still not well understood.…”

Section: Discussionmentioning

confidence: 99%

“…The instability of the diastolic resting state is thus well-known [ 61 – 63 ] and it plays an important role in the initiation of various cardiac arrhythmias [ 22 ]. However, the precise mechanistic relationship between Ca and dangerous AP repolarization is still not well understood.…”

Section: Discussionmentioning

confidence: 99%

Buffering and total calcium levels determine the presence of oscillatory regimes in cardiac cells

et al. 2020

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Calcium oscillations and waves induce depolarization in cardiac cells which are believed to cause life-threathening arrhythimas. In this work, we study the conditions for the appearance of calcium oscillations in both a detailed subcellular model of calcium dynamics and a minimal model that takes into account just the minimal ingredients of the calcium toolkit. To avoid the effects of homeostatic changes and the interaction with the action potential we consider the somewhat artificial condition of a cell without pacing and with no calcium exchange with the extracellular medium. Both the full subcellular model and the minimal model present the same scenarios depending on the calcium load: two stationary states, one with closed ryanodine receptors (RyR) and most calcium in the cell stored in the sarcoplasmic reticulum (SR), and another, with open RyRs and a depleted SR. In between, calcium oscillations may appear. The robustness of these oscillations is determined by the amount of calsequestrin (CSQ). The lack of this buffer in the SR enhances the appearance of oscillations. The minimal model allows us to relate the stability of the oscillating state to the nullcline structure of the system, and find that its range of existence is bounded by a homoclinic and a Hopf bifurcation, resulting in a sudden transition to the oscillatory regime as the cell calcium load is increased. Adding a small amount of noise to the RyR behavior increases the parameter region where oscillations appear and provides a gradual transition from the resting state to the oscillatory regime, as observed in the subcellular model and experimentally.

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Nonlinear onset of calcium wave propagation in cardiac cells

Cited by 7 publications

References 39 publications

Mechanism for Triggered Waves in Atrial Myocytes

Mechanism for Triggered Waves in Atrial Myocytes

Characteristics of cell motility during cell collision

Buffering and total calcium levels determine the presence of oscillatory regimes in cardiac cells

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