Noble1962_HodgkinHuxleyEquation
Ontology highlight
ABSTRACT:
SUBMITTER: 
Vijayalakshmi Chelliah
PROVIDER: MODEL8686121468 | BioModels | 2005-01-01
REPOSITORIES: BioModels
Publications
A modification of the Hodgkin--Huxley equations applicable to Purkinje fibre action and pace-maker potentials.
The Journal of physiology 19620201
Similar Datasets
Project description:This a model from the article:
Reconstruction of the electrical activity of cardiac Purkinje fibres.
McAllister RE, Noble D, Tsien RW. J Physiol.
1975; 251(1):1-59 1185607
,
Abstract:
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 the theoretical action potential is triggered by the onset of iX1, which becomes activated over the plateau range of potentials. iK2 also activates during the plateau but does not play a controlling role in the repolarization. Hwever, iK2 does govern the slow pace-maker depolarization through its subsequent deactivation at negative potentials. 4. The individual phases of the calculated action potential and their 'experimental' modifications were compared with published records. The upstroke is generated by a Hodgkin-Huxley type sodium conductance (gNa), and rises with a maximum rate of 478 V/sec, somewhat less than experimentally observed values ( up to 800 V/sec). The discrepancy is discussed in relation to experimental attempts at measuring gNa. 5. The ole of the transient outward chloride current (called igr) was studied in calculations of the rapid phase of repolarization and 'notch' configuration...
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
McAllister, Noble, Tsien.(1975) - version05
The original CellML model was created by:
Noble,Penny,J
penny.noble@dpag.ox.ac.uk
Department of Physiology, Anatomy & Genetics.
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 | MODEL9808533471 | 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: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:Noble rot results from atypical infections of ripe grape berries by Botrytis cinerea. Unlike bunch rot, noble rot promotes favorable changes in grape berries and accumulation of secondary metabolites that enhance wine grape quality. Noble rot-infected berries of Sémillon, a white-skinned variety, were collected over three years from a commercial vineyard at the same time fruit were harvested for botrytized wine production. Transcriptomic and metabolomic data were integrated to identify pathways associated with distinct stages of noble rot. Botrytis induced the expression of known key regulators of pathways in secondary metabolism associated with berry ripening. The activation by Botrytis during noble rot of metabolic pathways associated with berry ripening was further supported by comparisons with transcriptomes of red-skinned varieties at véraison. A prominent and common outcome of noble rot and berry ripening was the enhancement of the phenylpropanoid metabolism. Induced synthesis of stilbenes, flavonoids, and anthocyanins was supported by both transcriptional and metabolite analyses. Enzyme assays and targeted gene expression analyses of samples from the three distinct years confirmed that the activation of central and peripheral phenylpropanoid pathways is a consistent hallmark of noble rot. Finally, we show that the impact of noble rot on grape metabolism is still detectable in botrytized wines. These results demonstrate that despite the late stage of terminal senescence of a plant organ, a biotic stress can cause a major reprogramming of plant metabolism leading, in case of noble rot, to the synthesis of important metabolites for grape berry flavor and aroma.
2015-10-12 | GSE67932 | GEO
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model M-bM-^@M-^\single-type neuronM-bM-^@M-^]. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by M-bM-^@M-^\the neural communication systemM-bM-^@M-^] components. Pukinje cells and granule cell layer of the mouse cerebellum were collected by laser microdissection for RNA extraction and hybridization on Affymetrix microarrays.
2013-01-17 | E-GEOD-26749 | biostudies-arrayexpress
Project description:Noble rot results from atypical infections of ripe grape berries by Botrytis cinerea. Unlike bunch rot, noble rot promotes favorable changes in grape berries and accumulation of secondary metabolites that enhance wine grape quality. Noble rot-infected berries of Sémillon, a white-skinned variety, were collected over three years from a commercial vineyard at the same time fruit were harvested for botrytized wine production. Transcriptomic and metabolomic data were integrated to identify pathways associated with distinct stages of noble rot. Botrytis induced the expression of known key regulators of pathways in secondary metabolism associated with berry ripening. The activation by Botrytis during noble rot of metabolic pathways associated with berry ripening was further supported by comparisons with transcriptomes of red-skinned varieties at véraison. A prominent and common outcome of noble rot and berry ripening was the enhancement of the phenylpropanoid metabolism. Induced synthesis of stilbenes, flavonoids, and anthocyanins was supported by both transcriptional and metabolite analyses. Enzyme assays and targeted gene expression analyses of samples from the three distinct years confirmed that the activation of central and peripheral phenylpropanoid pathways is a consistent hallmark of noble rot. Finally, we show that the impact of noble rot on grape metabolism is still detectable in botrytized wines. These results demonstrate that despite the late stage of terminal senescence of a plant organ, a biotic stress can cause a major reprogramming of plant metabolism leading, in case of noble rot, to the synthesis of important metabolites for grape berry flavor and aroma. The experimental design consists of 4 treatments, berries at 3 distinct stages of noble rot and berries without apparent symptoms of infection. From each treatment a total of 4 biological replicates were sequenced with RNAseq, each replicate corresponded to independent pools of 10-15 berries harvested from adjacent grapevines.
2015-10-12 | E-GEOD-67932 | biostudies-arrayexpress
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model “single-type neuron”. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by “the neural communication system” components.
2013-01-17 | GSE26749 | GEO
Project description:This a model from the article:
Reconstruction of sino-atrial node pacemaker potential based on the voltage
clamp experiments.
Yanagihara K, Noma A, Irisawa H. Jpn J Physiol
1980;30(6):841-57 7265560
,
Abstract:
The pacemaker activity of the S-A node cell was explained by reconstructing the pacemaker potential using a Hodgkin-Huxley type mathematical model which was based on the reported voltage clamp data. In this model four dynamic currents, the sodium current iNa, the slow inward current, is, the potassium current, iK, and the hyperpolarization-activated current, ih, in addition to a time-dependent leak current, i1 were included. The model simulated the spontaneous action potential the current voltage relationship, and the voltage clamp experiment in normal Tyrode solution of the rabbit S-A node. Furthermore, the changes of activity induced by the potassium current blocker Ba2+, by applying constant current, acetylcholine, and epinephrine were also reconstructed. It was strongly suggested that the pacemaker depolarization in the S-A node cell is mainly due to a gradual increase of iS during diastole, and that the contribution of iK is much less compared to the potassium current iK2 in the Purkinje fiber pacemaker depolarization. The rising phase of the action potential was due to iS and the plateau phase is determined by both the inactivation of iS and activation of iK.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Yanagihara K, Noma A, Irisawa H. (1980) - version=1.0
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 | MODEL1006230072 | BioModels
Project description:Using a genetic model, we present a high resolution chromatin fibre analysis of transcriptionally active (Xa) and inactive (Xi) X chromosomes packaged into euchromatin and facultative heterochromatin. Our results show that gene promoters have an open chromatin structure that is enhanced upon transcriptional activation but the Xa and the Xi have similar overall 30-nm chromatin fibre structures. Therefore, the formation of facultative heterochromatin is dependent on factors that act at a level above the 30-nm fibre and transcription does not alter bulk chromatin fibre structures. However, large scale chromatin structures on Xa are decondensed compared to the Xi and transcription inhibition is sufficient to promote large scale chromatin compaction. We show a link between transcription and large scale chromatin packaging independent of the bulk 30-nm chromatin fibre and propose that transcription, not the global compaction of 30-nm chromatin fibres, determines the cytological appearance of large scale chromatin structures. This SuperSeries is composed of the SubSeries listed below.
2010-08-27 | GSE23818 | GEO
Project description:Emerging evidence suggests that estrogen and prolactin (PRL) play a key role in prostate cancer development, yet their relationship and molecular actions in prostate is not well understood. To address this issue, we made the first direct comparison of estrogen and PRL actions in the Noble rat (NBL) prostate dysplasia model.
2010-05-09 | GSE17819 | GEO