McAllister1975_CardiacPurkinjeFibres
Ontology highlight
ABSTRACT:
SUBMITTER: 
Vijayalakshmi Chelliah
PROVIDER: MODEL9808533471 | BioModels | 2005-01-01
REPOSITORIES: BioModels
Publications
Reconstruction of the electrical activity of cardiac Purkinje fibres.
McAllister R E RE Noble D D Tsien R W RW
The Journal of physiology 19750901 1
1. The electrical activity of Cardiac Purkinje fibres was reconstructed using a mathematical model of the membrane current. The individual components of ionic curent were described by equations which wee based as closely as possible on previous experiments using the voltage clamp technique. 2. Membrane action potentials and pace-maker activity were calculated and compared with time course of underlying changes in two functionally distinct outeard currents, iX1 and iK2. 3. The repolarization of t ...[more]
Similar Datasets
Project description:This a model from the article:
A modification of the Hodgkin--Huxley equations applicable to Purkinje fibre action and pace-maker potentials.
NOBLE D. J Physiol.
1962;160:317-52. 14480151
,
Abstract:
No Abstract Available
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble. (1962) - version05
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@auckland.ac.nz
The University of Auckland
Auckland Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL8686121468 | BioModels
Project description:This a model from the article:
A model of sino-atrial node electrical activity based on a modification of the DiFrancesco-Noble (1984) equations.
Noble D, Noble SJ. Proc R Soc Lond B Biol Sci.
1984 Sep 22;222(1228):295-304. 6149553
,
Abstract:
DiFrancesco & Noble's (1984) equations (Phil. Trans. R. Soc. Lond. B (in the press.] have been modified to apply to the mammalian sino-atrial node. The modifications are based on recent experimental work. The modified equations successfully reproduce action potential and pacemaker activity in the node. Slightly different versions have been developed for peripheral regions that show a maximum diastolic potential near --75 mV and for central regions that do not hyperpolarize beyond --60 to --65 mV. Variations in extracellular potassium influence the frequency of pacemaker activity in the s.a. node model very much less than they do in the Purkinje fibre model. This corresponds well to the experimental observation that the node is less sensitive to external [K] than are Purkinje fibres. Activation of the Na-K exchange pump in the model by increasing intracellular sodium can suppress pacemaker activity. This phenomenon may contribute to the mechanism of overdrive suppression.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble D, Noble SJ. (1984) - version04
The original CellML model was created by:
Noble, Penny, J
penny.noble@dpag.ox.ac.uk
Oxford University
Department of Physiology, Anatomy & Genetics
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL0406151557 | BioModels
Project description:This a model from the article:
A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction.
Luo CH, Rudy Y. Circ Res.
1991 Jun;68(6):1501-26. 1709839
,
Abstract:
A mathematical model of the membrane action potential of the mammalian ventricular cell is introduced. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. The time-independent potassium current, IK1, includes a negative-slope phase and displays significant crossover phenomenon as [K]o is varied. The time-dependent potassium current, IK, shows only a minimal degree of crossover. A novel potassium current that activates at plateau potentials is included in the model. The simulated action potential duplicates the experimentally observed effects of changes in [K]o on action potential duration and rest potential. Physiological simulations focus on the interaction between depolarization and repolarization (i.e., premature stimulation). Results demonstrate the importance of the slow recovery of INa in determining the response of the cell. Simulated responses to periodic stimulation include monotonic Wenckebach patterns and alternans at normal [K]o, whereas at low [K]o nonmonotonic Wenckebach periodicities, aperiodic patterns, and enhanced supernormal excitability that results in unstable responses ("chaotic activity") are observed. The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Luo CH, Rudy Y. (1991) - version06
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL0479527919 | BioModels
Project description:This is the model described in the article:
Reconstruction of the action potential of ventricular myocardial fibres.
Beeler GW, Reuter H. J Physiol.
1977 Jun;268(1):177-210. Pubmed ID: 874889
, full text
at PubMed central (PMCID:PMC1283659).
Abstract:
1. A mathematical model of membrane action potentials of mammalian ventricular myocardial fibres is described. The reconstruction model is based as closely as possible on ionic currents which have been measured by the voltage-clamp method.
2. Four individual components of ionic current were formulated mathematically in terms of Hodgkin-Huxley type equations. The model incorporates two voltage- and time-dependent inward currents, the excitatory inward sodium current, i(Na), and a secondary or slow inward current, i(s), primarily carried by calcium ions. A time-independent outward potassium current, i(K1), exhibiting inward-going rectification, and a voltage- and time-dependent outward current, i(x1), primarily carried by potassium ions, are further elements of the model.
3. The i(Na) is primarily responsible for the rapid upstroke of the action potential, while the other current components determine the configuration of the plateau of the action potential and the re-polarization phase. The relative importance of inactivation of i(s) and of activation of i(x1) for termination of the plateau is evaluated by the model.
4. Experimental phenomena like slow recovery of the sodium system from inactivation, frequency dependence of the action potential duration, all-or-nothing re-polarization, membrane oscillations are adequately described by the model.
5. Possible inadequacies and shortcomings of the model are discussed.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Beeler, Reuter, 1977 version 8
The original CellML model was created and curated by:
Catherine May Lloyd
c.lloyd(at)auckland.ac.nz
University of Auckland,
Auckland Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL7889395724 | BioModels
Project description:This a model from the article:
Mathematical models of the electrical action potential of Purkinje fibre cells.
Philip Stewart, Oleg V. Aslanidi, Denis Noble, Penelope J. Noble, Mark R. Boyett and Henggui Zhang. Phil. Trans. R. Soc. A
13 June 2009 vol. 367 no. 1896 2225-2255 doi:10.1098/rsta.2008.0283
,
Abstract:
Early development of ionic models for cardiac myocytes, from the pioneering modification of the Hodgkin–Huxley giant squid axon model by Noble to the iconic DiFrancesco–Noble model integrating voltage-gated ionic currents, ion pumps and exchangers, Ca2+ sequestration and Ca2+-induced Ca2+ release, provided a general description for a mammalian Purkinje fibre (PF) and the framework for modern cardiac models. In the past two decades, development has focused on tissue-specific models with an emphasis on the sino-atrial (SA) node, atria and ventricles, while the PFs have largely been neglected. However, achieving the ultimate goal of creating a virtual human heart will require detailed models of all distinctive regions of the cardiac conduction system, including the PFs, which play an important role in conducting cardiac excitation and ensuring the synchronized timing and sequencing of ventricular contraction. In this paper, we present details of our newly developed model for the human PF cell including validation against experimental data. Ionic mechanisms underlying the heterogeneity between the PF and ventricular action potentials in humans and other species are analysed. The newly developed PF cell model adds a new member to the family of human cardiac cell models developed previously for the SA node, atrial and ventricular cells, which can be incorporated into an anatomical model of the human heart with details of its electrophysiological heterogeneity and anatomical complexity.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
CellMLdetails
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230012 | BioModels
Project description:Drug-induced cardiac arrhythmia characterized by QT prolongation and torsade de pointes has been a major reason for drug withdrawal at the late stage of clinical trials. Current preclinical testing is still insufficient to identify drugs with pro-arrhythmic risks. Human induced pluripotent stem cell-derived cardiomyocytes are a promising development in safety screening as a reproducible human model. Using the patch-clamp technique, we showed that human induced pluripotent stem cell-derived cardiomyocytes exhibited spontaneous action potentials, which represent relatively immature forms of cardiac cells. Furthermore, in some spontaneously beating cells, a hERG blocker, E4031, depolarized membrane potentials and stopped spontaneous firing, resulting in failure to evaluate drug effects on electrophysiological parameters that reflect repolarization processes. Here we show that human stem cell-derived cardiomyocytes with transduced KCNJ2 encoding the inward-rectifier potassium channel have characteristics similar to mature cardiomyocytes including responsiveness to rate changes and potassium channel blockers. Our novel strategy could allow implementation of human induced pluripotent stem cell-derived cardiomyocytes in drug safety assessment for cardiac toxicity.
2017-06-20 | GSE63232 | GEO
Project description:Analysis of gene expression of mESC-derived cardiac purkinje fiber-like cells at mRNA level. Dysfunction of the cardiac conduction system (CCS) significantly impacts pathogenesis of arrhythmia, a major cause of morbidity and mortality. Strategies to derive cardiac conduction cells including Purkinje fiber cells (PC) would facilitate models for mechanistic studies and drug discovery, and also provide new cellular materials for regenerative therapies. A high-throughput chemical screen using CCS:lacZ and Contactin2:eGFP (Cntn2:eGFP) reporter embryonic stem cell (ESC) lines was used to discover a small molecule, sodium nitroprusside (SN), that efficiently promotes the generation of cardiac cells that express gene profiles and generate action potentials of PC-like cells. Imaging and mechanistic studies suggest that SN promotes the generation of PC from cardiac progenitors initially expressing cardiac myosin heavy chain, and that it does so by activating cAMP signaling. These findings provide a novel strategy to derive scalable PC, along with insight into the ontogeny of CCS development.
2016-04-20 | GSE68025 | GEO
Project description:Wang2008 - Mimicking the inhibitory effect of
riluzole on membrane conductance in skeletal fibres
This model is described in the article:
Riluzole-induced block of
voltage-gated Na+ current and activation of BKCa channels in
cultured differentiated human skeletal muscle cells.
Wang YJ, Lin MW, Lin AA, Wu
SN.
Life Sci. 2008 Jan; 82(1-2):
11-20
Abstract:
Riluzole is known to be of therapeutic use in the management
of amyotrophic lateral sclerosis. In this study, we
investigated the effects of riluzole on ion currents in
cultured differentiated human skeletal muscle cells (dHSkMCs).
Western blotting revealed the protein expression of
alpha-subunits for both large-conductance Ca2+-activated K+
(BK(Ca)) channel and Na+ channel (Na(v)1.5) in these cells.
Riluzole could reduce the frequency of spontaneous beating in
dHSkMCs. In whole-cell configuration, riluzole suppressed
voltage-gated Na+ current (I(Na)) in a concentration-dependent
manner with an IC50 value of 2.3 microM. Riluzole (10 microM)
also effectively increased Ca2+-activated K+ current (I(K(Ca)))
which could be reversed by iberiotoxin (200 nM) and paxilline
(1 microM), but not by apamin (200 nM). In inside-out patches,
when applied to the inside of the cell membrane, riluzole (10
microM) increased BK(Ca)-channel activity with a decrease in
mean closed time. Simulation studies also unraveled that both
decreased conductance of I(Na) and increased conductance of
I(K(Ca)) utilized to mimic riluzole actions in skeletal muscle
cells could combine to decrease the amplitude of action
potentials and increase the repolarization of action
potentials. Taken together, inhibition of I(Na) and stimulation
of BK(Ca)-channel activity caused by this drug are partly, if
not entirely, responsible for its muscle relaxant actions in
clinical setting.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000693.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2018-03-21 | BIOMD0000000693 | BioModels
Project description:This a model from the article:
Excitation-contraction coupling and extracellular calcium transients in rabbit
atrium: reconstruction of basic cellular mechanisms.
Hilgemann DW, Noble D. Proc R Soc Lond B Biol Sci
1987 Mar 23;230(1259):163-205 2884668
,
Abstract:
Interactions of electrogenic sodium-calcium exchange, calcium channel and
sarcoplasmic reticulum in the mammalian heart have been explored by simulation
of extracellular calcium transients measured with tetramethylmurexide in rabbit
atrium. The approach has been to use the simplest possible formulations of these
mechanisms, which together with a minimum number of additional mechanisms allow
reconstruction of action potentials, intracellular calcium transients and
extracellular calcium transients. A 3:1 sodium-calcium exchange stoichiometry is
assumed. Calcium-channel inactivation is assumed to take place by a
voltage-dependent mechanism, which is accelerated by a rise in intracellular
calcium; intracellular calcium release becomes a major physiological regulator
of calcium influx via calcium channels. A calcium release mechanism is assumed,
which is both calcium- and voltage-sensitive, and which undergoes prolonged
inactivation. 200 microM cytosolic calcium buffer is assumed. For most
simulations only instantaneous potassium conductances are simulated so as to
study the other mechanisms independently of time- and calcium-dependent outward
current. Thus, the model reconstructs extracellular calcium transients and
typical action-potential configuration changes during steady-state and
non-steady-state stimulation from the mechanisms directly involved in
trans-sarcolemmal calcium movements. The model predicts relatively small
trans-sarcolemmal calcium movements during regular stimulation (ca. 2 mumol kg-1
fresh mass per excitation); calcium current is fully activated within 2 ms of
excitation, inactivation is substantially complete within 30 ms, and
sodium-calcium exchange significantly resists repolarization from approximately
-30 mV. Net calcium movements many times larger are possible during
non-steady-state stimulation. Long action potentials at premature excitations or
after inhibition of calcium release can be supported almost exclusively by
calcium current (net calcium influx 5-30 mumol kg-1 fresh mass); action
potentials during potentiated post-stimulatory contractions can be supported
almost exclusively by sodium-calcium exchange (net calcium efflux 4-20 mumol
kg-1 fresh mass). Large calcium movements between the extracellular space and
the sarcoplasmic reticulum can take place through the cytosol with virtually no
contractile activation. The simulations provide integrated explanations of
electrical activity, contractile function and trans-sarcolemmal calcium
movements, which were outside the explanatory range of previous models.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Hilgemann DW, Noble D. (1987) - version06
The original CellML model was created by:
Noble, Penny, J
penny.noble@dpag.ox.ac.uk
Oxford University
Department of Physiology, Anatomy & Genetics
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL0848444339 | BioModels
Project description:This a model from the article:
Contributions of HERG K+ current to repolarization of the human ventricular
action potential.
Fink M, Noble D, Virag L, Varro A, Giles WR. Prog Biophys Mol Biol
2008 Jan-Apr;96(1-3):357-76 17919688
,
Abstract:
Action potential repolarization in the mammalian heart is governed by
interactions of a number of time- and voltage-dependent channel-mediated
currents, as well as contributions from the Na+/Ca2+ exchanger and the Na+/K+
pump. Recent work has shown that one of the K+ currents (HERG) which contributes
to repolarization in mammalian ventricle is a locus at which a number of point
mutations can have significant functional consequences. In addition, the
remarkable sensitivity of this K+ channel isoform to inhibition by a variety of
pharmacological agents and clinical drugs has resulted in HERG being a major
focus for Safety Pharmacology requirements. For these reasons we and others have
attempted to define the functional role for HERG-mediated K+ currents in
repolarization of the action potential in the human ventricle. Here, we describe
and evaluate changes in the formulations for two K+ currents, IK1 and HERG (or
IK,r), within the framework of ten Tusscher model of the human ventricular
action potential. In this computational study, new mathematical formulations for
the two nonlinear K+ conductances, IK1 and HERG, have been developed based upon
experimental data obtained from electrophysiological studies of excised human
ventricular tissue and/or myocytes. The resulting mathematical model provides
much improved simulations of the relative sizes and time courses of the K+
currents which modulate repolarization. Our new formulation represents an
important first step in defining the mechanism(s) of repolarization of the
membrane action potential in the human ventricle. Our overall goal is to
understand the genesis of the T-wave of the human electrocardiogram.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Fink M, Noble D, Virag L, Varro A, Giles WR. (2008) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230009 | BioModels