Bondarenko, Szigeti, Bett, Kim, Rasmusson, 2004
This CellML model runs in both OpenCell and COR to reproduce the the action potential traces from Figure 16 of the publication. This model represents the APICAL CELL variant as described in Bondarenko et al.'s 2004 paper.
ABSTRACT: We have developed a mathematical model of the mouse ventricular myocyte action potential (AP) from voltage-clamp data of the underlying currents and Ca2+ transients. Wherever possible, we used Markov models to represent the molecular structure and function of ion channels. The model includes detailed intracellular Ca2+ dynamics, with simulations of localized events such as sarcoplasmic Ca2+ release into a small intracellular volume bounded by the sarcolemma and sarcoplasmic reticulum. Transporter-mediated Ca2+ fluxes from the bulk cytosol are closely matched to the experimentally reported values and predict stimulation rate-dependent changes in Ca2+ transients. Our model reproduces the properties of cardiac myocytes from two different regions of the heart: the apex and the septum. The septum has a relatively prolonged AP, which reflects a relatively small contribution from the rapid transient outward K+ current in the septum. The attribution of putative molecular bases for several of the component currents enables our mouse model to be used to simulate the behavior of genetically modified transgenic mice.
The original paper reference is cited below:
Computer model of action potential of mouse ventricular myocytes, Vladimir E. Bondarenko, Gyula P. Szigeti, Glenna C. L. Bett, Song-Jung Kim, and Randall L. Rasmusson, 2004, American Journal of Physiology, 287, H1378-H1403. PubMed ID: 15142845
|Schematic diagram of the mouse model ionic currents and calcium fluxes.|
|State diagram of the Markov model for the sodium channel. CNa denotes a closed channel state, ONa is the open state, IFNa represents the fast, inactivated state, I1Na and I2Na are the intermediate inactivated states, and IC2Na and IC3Na are the closed-inactivation states.|