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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 | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000045?filename=BIOMD0000000045-biopax2.owl	Owl
	BIOMD0000000045?filename=BIOMD0000000045-biopax3.owl	Owl
	BIOMD0000000045?filename=BIOMD0000000045-matlab.m	Other
	BIOMD0000000045?filename=BIOMD0000000045-octave.m	Other
	BIOMD0000000045?filename=BIOMD0000000045.m	Other

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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 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 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.

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