A compartment model with variable ion channel density on the propagation of action potentials along a nonuniform axon

2012 ◽  
Vol 85 (12) ◽  
Author(s):  
D. Lee ◽  
S.-G. Lee ◽  
S. Kim
Keyword(s):  
Ion Channel ◽  
Action Potentials ◽  
Compartment Model ◽  
Channel Density

MODELING OF WOLFF–PARKINSON–WHITE SYNDROME

2003 ◽  
Vol 13 (12) ◽  
pp. 3827-3834
Author(s):  
ROBERT HINCH
Keyword(s):  
Asymptotic Analysis ◽  
Ion Channel ◽  
Sodium Channel ◽  
Channel Model ◽  
Accessory Pathway ◽  
Simplified Model ◽  
Channel Kinetics ◽  
White Syndrome ◽  
Channel Density ◽  
Wolff Parkinson White Syndrome

Wolff–Parkinson–White syndrome is a disease where an arrhythmia is caused by the ventricles being electrically excited by an additional accessory pathway that links the atria to the ventricles. The spread of the activation wave from this pathway to the ventricles is modeled using a simplified model of Hodgkin–Huxley sodium channel kinetics, in a two ion-channel model. The model is investigated both analytically (using an asymptotic analysis) and numerically, and both methods are shown to give the same result. It is found that for a given width of the accessory pathway, there is a critical sodium channel density needed for the activation wave to spread from the pathway to the tissue. This result provides an explanation for the success of class-I anti-arrhythmic drugs in treating Wolff–Parkinson–White syndrome.

scholarly journals Cardiac Transmembrane Ion Channels and Action Potentials: Cellular Physiology and Arrhythmogenic Behavior

2020 ◽  
Author(s):  
András Varró ◽  
Jakub Tomek ◽  
Norbert Nagy ◽  
Laszlo Virag ◽  
Elisa Passini ◽  
...  
Keyword(s):  
Ion Channel ◽  
Action Potentials ◽  
Cardiac Electrophysiology ◽  
Current Knowledge ◽  
Animal Experiments ◽  
Cardiac Cells ◽  
Cellular Mechanisms ◽  
Electrophysiological Properties ◽  
Channel Expression ◽  
Ionic Mechanisms

Cardiac arrhythmias are among the leading causes of mortality. They often arise from alterations in the electrophysiological properties of cardiac cells, and their underlying ionic mechanisms. It is therefore critical to further unravel the patho-physiology of the ionic basis of human cardiac electrophysiology in health and disease. In the first part of this review, current knowledge on the differences in ion channel expression and properties of the ionic processes that determine the morphology and properties of cardiac action potentials and calcium dynamics from cardiomyocytes in different regions of the heart are described. Then the cellular mechanisms promoting arrhythmias in congenital or acquired conditions of ion channel function (electrical remodelling) are discussed. The focus is human relevant findings obtained with clinical, experimental and computational studies, given that interspecies differences make the extrapolation from animal experiments to the human clinical settings difficult. Deepening the understanding of the diverse patholophysiology of human cellular electrophysiology will help developing novel and effective antiarrhythmic strategies for specific subpopulations and disease conditions.

Reduction of the Diffusion Equations of Ion Channel Clusters with Virtually No Increase in the Error Bound

2020 ◽  
pp. 2150035
Author(s):  
Marifi Güler
Keyword(s):  
Ion Channel ◽  
Error Bound ◽  
Density Fluctuations ◽  
Diffusion Equations ◽  
Channel Density ◽  
Differential Formulation ◽  
Excitable Membranes ◽  
White Noises ◽  
Structural Simplicity ◽  
Strong Diffusion

A stochastic differential formulation for the collective dynamics of ion channel clusters in excitable membranes is developed from the so-called “reduced strong diffusion formulation”. In this error bound optimizing reduced formulation, the potassium channel states [Formula: see text] and [Formula: see text], and, the sodium channel states [Formula: see text] and [Formula: see text] are the retained states; consequently, the formulation accommodates only four channel variables and five white noises. The accuracy of the formulation is tested over the standard deviations and autocorrelation times of the channel density fluctuations. The findings are seen to be virtually identical to the corresponding results from the exact microscopic Markov simulations. The formulation arises as the most accurate model with that structural simplicity, thus making it an important model for both analytic analyses and numerical simulations in the study of finite-sized membranes.

scholarly journals Critical behavior in the artificial axon

2021 ◽  
Author(s):  
Ziqi Pi ◽  
Giovanni Zocchi
Keyword(s):  
Ion Channel ◽  
Critical Behavior ◽  
Delay Time ◽  
Action Potentials ◽  
Scaling Exponent ◽  
Saddle Node Bifurcation ◽  
Channel Dynamics ◽  
A Cell ◽  
Universal Properties ◽  
Fast Ion

Abstract The Artificial Axon is a unique synthetic system, based on biomolecular components, which supports action potentials. Here we examine, experimentally and theoretically, the properties of the threshold for firing in this system. As in real neurons, this threshold corresponds to the critical point of a saddle-node bifurcation. We measure the delay time for firing as a function of the distance to threshold, recovering the expected scaling exponent of −1/2. We introduce a minimal model of the Morris-Lecar type, validate it on the experiments, and use it to extend analytical results obtained in the limit of ”fast” ion channel dynamics. In particular, we discuss the dependence of the firing threshold on the number of channels. The Artificial Axon is a simplified system, an Ur-neuron, relying on only one ion channel species for functioning. Nonetheless, universal properties such as the action potential behavior near threshold are the same as in real neurons. Thus we may think of the Artificial Axon as a cell-free breadboard for electrophysiology research.

Relationship between energy expenditure and ion channel density in the turtle and rat brain

1989 ◽  
Vol 257 (6) ◽  
pp. R1354-R1358 ◽  
Author(s):  
R. A. Edwards ◽  
P. L. Lutz ◽  
D. G. Baden
Keyword(s):  
Energy Consumption ◽  
Energy Expenditure ◽  
Ion Channel ◽  
Rat Brain ◽  
Receptor Interaction ◽  
Na Channel ◽  
Apparent Difference ◽  
Na Channels ◽  
Channel Density ◽  
Rat Synaptosomes

Synaptosomes were isolated from turtle and rat brains to determine whether differences in brain ion channel densities accounted for the turtle's ability to survive anoxia compared with the mammal. The Na(+)-channel binding neurotoxin brevetoxin showed high-affinity specific binding in both turtle and rat synaptosomes, suggesting specific ligand-receptor interaction. The maximum binding capacity (Bmax) value for the turtle was only about one-third of that found for the rat synaptosomes, suggesting that the turtle synaptosome has a correspondingly lower Na+ channel density than the rat. This apparent difference in Na+ channel density is not reflected in metabolic rates, since at the same temperature (31 degrees C) the O2 consumption of both the rat and turtle synaptosome was almost identical. The large reductions in energy expenditure seen in synaptosomes incubated in Na(+)-free media and in media containing ouabain (approximately 50% turtle, 80% rat) are probably related to the halting of transmembrane Na(+)-K+ exchange. The greater reduction in the rat may be related to the apparent greater density of Na+ channels in the rat brain. However, compared with the 90% reduction in brain metabolism that occurs when the turtle brain becomes anoxic, the differences in ion channel density and in the costs of ion pumping between the rat and turtle brain are trivial. Closing Na+ channels with tetrodotoxin and increasing Na+ channel activation with veratridine caused substantial decreases and increases in synaptosome energy consumption, respectively. This suggests that the modulation of ion channel conductance has a significant effect on metabolic cost and may be an important mechanism to reduce energy consumption and electrical activity in the anoxic turtle brain, while still maintaining ionic gradients.

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