Dataset Information

Kummer2000 - Oscillations in Calcium Signalling

ABSTRACT: Kummer2000 - Oscillations in Calcium Signalling Simplified (3-variable) calcium oscillation model Kummer et al. (2000) Biophys. J. 79, 1188-1195 This model is defined in a small compartment with low concentrations. You can run it first with the LSODA ODE solver and then with the Gillespie Monte Carlo method (in Time Course widget). This illustrates that at low particle numbers, as here, the stochastic simulation and the ODE approach produce different results (the stochastic approach is more correct in these circumstances). This file also demonstrates the use of several different plots to visualize results, including a histogram. This model is described in the article: Switching from simple to complex oscillations in calcium signaling. Kummer U, Olsen LF, Dixon CJ, Green AK, Bornberg-Bauer E, Baier G. Biophys. J. 2000 Sep; 79(3): 1188-1195 Abstract: We present a new model for calcium oscillations based on experiments in hepatocytes. The model considers feedback inhibition on the initial agonist receptor complex by calcium and activated phospholipase C, as well as receptor type-dependent self-enhanced behavior of the activated G(alpha) subunit. It is able to show simple periodic oscillations and periodic bursting, and it is the first model to display chaotic bursting in response to agonist stimulations. Moreover, our model offers a possible explanation for the differences in dynamic behavior observed in response to different agonists in hepatocytes. This model is hosted on BioModels Database and identified by: BIOMD0000000329. 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: Vijayalakshmi Chelliah

PROVIDER: BIOMD0000000329 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000329?filename=BIOMD0000000329-biopax2.owl	Owl
	BIOMD0000000329?filename=BIOMD0000000329-biopax3.owl	Owl
	BIOMD0000000329?filename=BIOMD0000000329-matlab.m	Other
	BIOMD0000000329?filename=BIOMD0000000329-octave.m	Other
	BIOMD0000000329?filename=BIOMD0000000329.m	Other

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Publications

Switching from simple to complex oscillations in calcium signaling.

Kummer U U Olsen L F LF Dixon C J CJ Green A K AK Bornberg-Bauer E E Baier G G

Biophysical journal 20000901 3

We present a new model for calcium oscillations based on experiments in hepatocytes. The model considers feedback inhibition on the initial agonist receptor complex by calcium and activated phospholipase C, as well as receptor type-dependent self-enhanced behavior of the activated G(alpha) subunit. It is able to show simple periodic oscillations and periodic bursting, and it is the first model to display chaotic bursting in response to agonist stimulations. Moreover, our model offers a possible ...[more]

PMID: 10968983

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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: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.

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