Model of arrhythmias in a cardiac cells network (Casaleggio et al. 2014)

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Accession:150691
" ... Here we explore the possible processes leading to the occasional onset and termination of the (usually) non-fatal arrhythmias widely observed in the heart. Using a computational model of a two-dimensional network of cardiac cells, we tested the hypothesis that an ischemia alters the properties of the gap junctions inside the ischemic area. ... In conclusion, our model strongly supports the hypothesis that non-fatal arrhythmias can develop from post-ischemic alteration of the electrical connectivity in a relatively small area of the cardiac cell network, and suggests experimentally testable predictions on their possible treatments."
Reference:
1 . Casaleggio A, Hines ML, Migliore M (2014) Computational model of erratic arrhythmias in a cardiac cell network: the role of gap junctions. PLoS One 9:e100288 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network; Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Cardiac ventricular cell;
Channel(s): I K; I Sodium; I Calcium; I Potassium;
Gap Junctions: Gap junctions;
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Spatio-temporal Activity Patterns; Detailed Neuronal Models; Action Potentials; Heart disease; Conductance distributions;
Implementer(s): Hines, Michael [Michael.Hines at Yale.edu]; Migliore, Michele [Michele.Migliore at Yale.edu];
Search NeuronDB for information about:  I K; I Sodium; I Calcium; I Potassium;
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