Dataset Information

Borghans1997 - Calcium Oscillation - Model 3

ABSTRACT: Borghans1997 - Calcium Oscillation - Model 3 A theoretical expoloration of possible mechanisms of intracellular calcium oscillations has been studied, considering three hypothesis. This model corresponds to the third hypothesis. This model is described in the article: Complex intracellular calcium oscillations. A theoretical exploration of possible mechanisms. Borghans JM, Dupont G, Goldbeter A. Biophys. Chem. 1997 May; 66(1): 25-41 Abstract: Intracellular Ca(2+) oscillations are commonly observed in a large number of cell types in response to stimulation by an extracellular agonist. In most cell types the mechanism of regular spiking is well understood and models based on Ca(2+)-induced Ca(2+) release (CICR) can account for many experimental observations. However, cells do not always exhibit simple Ca(2+) oscillations. In response to given agonists, some cells show more complex behaviour in the form of bursting, i.e. trains of Ca(2+) spikes separated by silent phases. Here we develop several theoretical models, based on physiologically plausible assumptions, that could account for complex intracellular Ca(2+) oscillations. The models are all based on one- or two-pool models based on CICR. We extend these models by (i) considering the inhibition of the Ca(2+)-release channel on a unique intracellular store at high cytosolic Ca(2+) concentrations, (ii) taking into account the Ca(2+)-activated degradation of inositol 1,4,5-trisphosphate (IP(3)), or (iii) considering explicity the evolution of the Ca(2+) concentration in two different pools, one sensitive and the other one insensitive to IP(3). Besides simple periodic oscillations, these three models can all account for more complex oscillatory behaviour in the form of bursting. Moreover, the model that takes the kinetics of IP(3) into account shows chaotic behaviour. This model is hosted on BioModels Database and identified by: MODEL6623009547 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . 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.

SUBMITTER: Harish Dharuri

PROVIDER: BIOMD0000000045 | BioModels | 2005-07-08

REPOSITORIES: BioModels

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Publications

Complex intracellular calcium oscillations. A theoretical exploration of possible mechanisms.

Borghans J M JM Dupont G G Goldbeter A A

Biophysical chemistry 19970501 1

Intracellular Ca(2+) oscillations are commonly observed in a large number of cell types in response to stimulation by an extracellular agonist. In most cell types the mechanism of regular spiking is well understood and models based on Ca(2+)-induced Ca(2+) release (CICR) can account for many experimental observations. However, cells do not always exhibit simple Ca(2+) oscillations. In response to given agonists, some cells show more complex behaviour in the form of bursting, i.e. trains of Ca(2+ ...[more]

PMID: 17029867

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Project description:Borghans1997 - Calcium Oscillation - Model 1 A theoretical expoloration of possible mechanisms of intracellular calcium oscillations has been studied, considering three hypothesis (see below). This model corresponds to the first hypothesis. This model is described in the article: Complex intracellular calcium oscillations. A theoretical exploration of possible mechanisms. Borghans JM, Dupont G, Goldbeter A. Biophys. Chem. 1997 May; 66(1): 25-41 Abstract: Intracellular Ca(2+) oscillations are commonly observed in a large number of cell types in response to stimulation by an extracellular agonist. In most cell types the mechanism of regular spiking is well understood and models based on Ca(2+)-induced Ca(2+) release (CICR) can account for many experimental observations. However, cells do not always exhibit simple Ca(2+) oscillations. In response to given agonists, some cells show more complex behaviour in the form of bursting, i.e. trains of Ca(2+) spikes separated by silent phases. Here we develop several theoretical models, based on physiologically plausible assumptions, that could account for complex intracellular Ca(2+) oscillations. The models are all based on one- or two-pool models based on CICR. We extend these models by (i) considering the inhibition of the Ca(2+)-release channel on a unique intracellular store at high cytosolic Ca(2+) concentrations, (ii) taking into account the Ca(2+)-activated degradation of inositol 1,4,5-trisphosphate (IP(3)), or (iii) considering explicity the evolution of the Ca(2+) concentration in two different pools, one sensitive and the other one insensitive to IP(3). Besides simple periodic oscillations, these three models can all account for more complex oscillatory behaviour in the form of bursting. Moreover, the model that takes the kinetics of IP(3) into account shows chaotic behaviour. This model is hosted on BioModels Database and identified by: MODEL6622689184 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . 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.

Project description:Borghans1997 - Calcium Oscillation - Model 2 A theoretical expoloration of possible mechanisms of intracellular calcium oscillations has been studied, considering three hypothesis (see below). This model corresponds to the second hypothesis. This model is described in the article: Complex intracellular calcium oscillations. A theoretical exploration of possible mechanisms. Borghans JM, Dupont G, Goldbeter A. Biophys. Chem. 1997 May; 66(1): 25-41 Abstract: Intracellular Ca(2+) oscillations are commonly observed in a large number of cell types in response to stimulation by an extracellular agonist. In most cell types the mechanism of regular spiking is well understood and models based on Ca(2+)-induced Ca(2+) release (CICR) can account for many experimental observations. However, cells do not always exhibit simple Ca(2+) oscillations. In response to given agonists, some cells show more complex behaviour in the form of bursting, i.e. trains of Ca(2+) spikes separated by silent phases. Here we develop several theoretical models, based on physiologically plausible assumptions, that could account for complex intracellular Ca(2+) oscillations. The models are all based on one- or two-pool models based on CICR. We extend these models by (i) considering the inhibition of the Ca(2+)-release channel on a unique intracellular store at high cytosolic Ca(2+) concentrations, (ii) taking into account the Ca(2+)-activated degradation of inositol 1,4,5-trisphosphate (IP(3)), or (iii) considering explicity the evolution of the Ca(2+) concentration in two different pools, one sensitive and the other one insensitive to IP(3). Besides simple periodic oscillations, these three models can all account for more complex oscillatory behaviour in the form of bursting. Moreover, the model that takes the kinetics of IP(3) into account shows chaotic behaviour. This model is hosted on BioModels Database and identified by: MODEL6622948601 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . 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.

Project description:Wang2007 - ATP induced intracellular Calicum Oscillation The model simulate the ATP-induced intracellular Ca2+ oscillations and the quantitative effect of ATP concentration on the oscillation characteristics such as the duration, peak concentration of intracellular Ca2+ and average interval. This model is described in the article: A quantitative kinetic model for ATP-induced intracellular Ca2+ oscillations. Wang J, Huang X, Huang W. J. Theor. Biol. 2007 Apr; 245(3): 510-519 Abstract: A quantitative kinetic model is proposed to simulate the ATP-induced intracellular Ca(2+) oscillations. The quantitative effect of ATP concentration upon the oscillations was successfully simulated. Our simulation results support previous experimental explanations that the Ca(2+) oscillations are mainly due to interaction of Ca(2+) release from the endoplasmic reticulum (ER) and the ATP-dependent Ca(2+) pump back into the ER, and the oscillations are prolonged by extracellular Ca(2+) entry that maintains the constant Ca(2+) supplies to its intracellular stores. The model is also able to simulate the sudden disappearance phenomenon of the Ca(2+) oscillations observed in some cell types by taking into account of the biphasic characteristic of the Ca(2+) release from the endoplasmic reticulum (ER). Moreover, the model simulation results for the Ca(2+) oscillations characteristics such as duration, peak [Ca(2+)](cyt), and average interval, etc., lead to prediction of some possible factors responsible for the variations of Ca(2+) oscillations in different types of cells. This model is hosted on BioModels Database and identified by: BIOMD0000000145. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. 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.

Project description:This a model from the article: A biophysically based mathematical model of unitary potential activity in interstitial cells of Cajal. Faville RA, Pullan AJ, Sanders KM, Smith NP. Biophys J 2008 Jul;95(1):88-104 18339738 , Abstract: Unitary potential (UP) depolarizations are the basic intracellular events responsible for pacemaker activity in interstitial cells of Cajal (ICCs), and are generated at intracellular sites termed "pacemaker units". In this study, we present a mathematical model of the transmembrane ion flows and intracellular Ca(2+) dynamics from a single ICC pacemaker unit acting at near-resting membrane potential. This model quantitatively formalizes the framework of a novel ICC pacemaking mechanism that has recently been proposed. Model simulations produce spontaneously rhythmic UP depolarizations with an amplitude of approximately 3 mV at a frequency of 0.05 Hz. The model predicts that the main inward currents, carried by a Ca(2+)-inhibited nonselective cation conductance, are activated by depletion of sub-plasma-membrane [Ca(2+)] caused by sarcoendoplasmic reticulum calcium ATPase Ca(2+) sequestration. Furthermore, pacemaker activity predicted by our model persists under simulated voltage clamp and is independent of [IP(3)] oscillations. The model presented here provides a basis to quantitatively analyze UP depolarizations and the biophysical mechanisms underlying their production. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Faville RA, Pullan AJ, Sanders KM, Smith NP. (2008) - version02 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.

Dataset Information

Borghans1997 - Calcium Oscillation - Model 3

Publications

Complex intracellular calcium oscillations. A theoretical exploration of possible mechanisms.

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