Dataset Information

Golomb2006_SomaticBursting_nonzero[Ca]

ABSTRACT: Model is according to the paper Contribution of Persistent Na+ Current and M-Type K+ Current to Somatic Bursting in CA1 Pyramidal Cell: Combined Experimental. This is the second model from this paper for the non-zero [Ca2+] initial value, parameters and the kinetics quations from Table2 in the paper. Figure9Aa has been reproduced by MathSBML. The original model from ModelDB. http://senselab.med.yale.edu/modeldb/ 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.

SUBMITTER: Enuo He

PROVIDER: BIOMD0000000119 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000119?filename=BIOMD0000000119-biopax2.owl	Owl
	BIOMD0000000119?filename=BIOMD0000000119-biopax3.owl	Owl
	BIOMD0000000119?filename=BIOMD0000000119-matlab.m	Other
	BIOMD0000000119?filename=BIOMD0000000119-octave.m	Other
	BIOMD0000000119?filename=BIOMD0000000119.m	Other

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Publications

Contribution of persistent Na+ current and M-type K+ current to somatic bursting in CA1 pyramidal cells: combined experimental and modeling study.

Golomb David D Yue Cuiyong C Yaari Yoel Y

Journal of neurophysiology 20060628 4

The intrinsic firing modes of adult CA1 pyramidal cells vary along a continuum of "burstiness" from regular firing to rhythmic bursting, depending on the ionic composition of the extracellular milieu. Burstiness is low in neurons exposed to a normal extracellular Ca(2+) concentration ([Ca(2+)](o)), but is markedly enhanced by lowering [Ca(2+)](o), although not by blocking Ca(2+) and Ca(2+)-activated K(+) currents. We show, using intracellular recordings, that burstiness in low [Ca(2+)](o) persis ...[more]

PMID: 16807352

Similar Datasets

Project description:This is the model without the slow potassium current, model 1, described in the article: Models of respiratory rhythm generation in the pre-Bötzinger complex. I. Bursting pacemaker neurons. Butera RJ Jr, Rinzel J, Smith JC. J Neurophysiol. 1999 Jul;82(1):382-97. Pubmed ID: 10400966 , full text at the Journal of Neurophysiology . Abstract: A network of oscillatory bursting neurons with excitatory coupling is hypothesized to define the primary kernel for respiratory rhythm generation in the pre-Bötzinger complex (pre-BötC) in mammals. Two minimal models of these neurons are proposed. In model 1, bursting arises via fast activation and slow inactivation of a persistent Na+ current INaP-h. In model 2, bursting arises via a fast-activating persistent Na+ current INaP and slow activation of a K+ current IKS. In both models, action potentials are generated via fast Na+ and K+ currents. The two models have few differences in parameters to facilitate a rigorous comparison of the two different burst-generating mechanisms. Both models are consistent with many of the dynamic features of electrophysiological recordings from pre-BötC oscillatory bursting neurons in vitro, including voltage-dependent activity modes (silence, bursting, and beating), a voltage-dependent burst frequency that can vary from 0.05 to > 1 Hz, and a decaying spike frequency during bursting. These results are robust and persist across a wide range of parameter values for both models. However, the dynamics of model 1 are more consistent with experimental data in that the burst duration decreases as the baseline membrane potential is depolarized and the model has a relatively flat membrane potential trajectory during the interburst interval. We propose several experimental tests to demonstrate the validity of either model and to differentiate between the two mechanisms. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Butera, Rinzel, Smith, 1999 version 05 The original CellML model was created and curated by: Catherine May Lloyd c.lloyd(at)auckland.ac.nz The University of 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.

Project description:This a model from the article: Effects of extracellular calcium on electrical bursting and intracellular and luminal calcium oscillations in insulin secreting pancreatic beta-cells. Chay TR Biophys J.1997 Sep;73(3):1673-88. 9284334, Abstract: The extracellular calcium concentration has interesting effects on bursting of pancreatic beta-cells. The mechanism underlying the extracellular Ca2+ effect is not well understood. By incorporating a low-threshold transient inward current to the store-operated bursting model of Chay, this paper elucidates the role of the extracellular Ca2+ concentration in influencing electrical activity, intracellular Ca2+ concentration, and the luminal Ca2+ concentration in the intracellular Ca2+ store. The possibility that this inward current is a carbachol-sensitive and TTX-insensitive Na+ current discovered by others is discussed. In addition, this paper explains how these three variables respond when various pharmacological agents are applied to the store-operated model. This model was taken from the CellML repository and automatically converted to SBML. The original model was: Chay TR (1997) - version05 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. For more information see the terms of use. 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.

Project description:Whereas cloning mammals by direct somatic cell nuclear transfer has been successful using a wide range of donor cell types, neurons from adult brain remain M-bM-^@M-^\unclonableM-bM-^@M-^] for unknown reasons. Here we examined whether neurons from adult mice could be cloned, using a combination of two epigenetic approaches. First, we used a specific antibody to discover cell types with reduced amounts of a repressive histone mark - dimethylated histone H3 lysine 9 (H3K9me2) - and identified CA1 pyramidal cells in the hippocampus and Purkinje cells in the cerebellum as candidates. Second, reconstructed embryos were treated with trichostatin A (TSA), a potent histone deacetylase inhibitor. Using CA1 cells, cloned offspring were obtained at high rates, reaching 10.2% and 4.6% (per embryos transferred) for male and female donors, respectively. Cerebellar Purkinje cell nuclei were too large to maintain their genetic integrity during nuclear transfer, leading to developmental arrest of embryos. However, gene expression analysis using cloned blastocysts corroborated a high rate of genomic reprogrammability of CA1 pyramidal and Purkinje cells. Neurons from the hippocampal dentate gyrus and cerebral cortex, which had higher amounts of H3K9me2, could also be used for producing cloned offspring, but the efficiencies were low. A more thorough analysis revealed that TSA treatment was essential for cloning adult neuronal cells. This study demonstrated for the first time that adult neurons could be cloned by nuclear transfer. Furthermore, our data imply that reduced amounts of H3K9me2 and increased histone acetylation appear to act synergistically to improve the development of cloned embryos. Comparative gene expression analyses using blastocysts of cloned embryos were performed by microarray. Cloned embryos were produced with three different types of donor cells (neonatal Sertoli cells, CA1 pyramidal cells and Purkinje cells) and all cloned embryos were treated with Trichostatin A (TSA). Each embryos were cultured for 96 h and blastocysts derived from each donor cell types were subjected to gene expression microarray. For comparison of gene expression, the data sets of control sex- and genotype-matched embryos produced by in vitro fertilization and SCNT-derived blastocysts from cumulus cells treated with TSA from our previous paper (Inoue K. et al. Science 2010) were also used.