ABSTRACT:
This a model from the article:
Evidence that calcium release-activated current mediates the biphasic electrical
activity of mouse pancreatic beta-cells.
Mears D, Sheppard NF Jr, Atwater I, Rojas E, Bertram R, Sherman A.
J Membr Biol1997 Jan 1;155(1):47-59
9002424,
Abstract:
The electrical response of pancreatic beta-cells to step increases in glucose
concentration is biphasic, consisting of a prolonged depolarization with action
potentials (Phase 1) followed by membrane potential oscillations known as
bursts. We have proposed that the Phase 1 response results from the combined
depolarizing influences of potassium channel closure and an inward, nonselective
cation current (ICRAN) that activates as intracellular calcium stores empty
during exposure to basal glucose (Bertram et al., 1995). The stores refill
during Phase 1, deactivating ICRAN and allowing steady-state bursting to
commence. We support this hypothesis with additional simulations and
experimental results indicating that Phase 1 duration is sensitive to the
filling state of intracellular calcium stores. First, the duration of the Phase
1 transient increases with duration of prior exposure to basal (2.8 mM) glucose,
reflecting the increased time required to fill calcium stores that have been
emptying for longer periods. Second, Phase 1 duration is reduced when islets are
exposed to elevated K+ to refill calcium stores in the presence of basal
glucose. Third, when extracellular calcium is removed during the basal glucose
exposure to reduce calcium influx into the stores, Phase 1 duration increases.
Finally, no Phase 1 is observed following hyperpolarization of the beta-cell
membrane with diazoxide in the continued presence of 11 mm glucose, a condition
in which intracellular calcium stores remain full. Application of carbachol to
empty calcium stores during basal glucose exposure did not increase Phase 1
duration as the model predicts. Despite this discrepancy, the good agreement
between most of the experimental results and the model predictions provides
evidence that a calcium release-activated current mediates the Phase 1
electrical response of the pancreatic beta-cell.
This model was taken from the
CellML repository and automatically converted to SBML.
The original model was:
Mears D, Sheppard NF Jr, Atwater I, Rojas E, Bertram R, Sherman A. (1997) - version=1.0
The original CellML model was created by:
Tessa Paris
tpar054@aucklanduni.ac.uk
The University of Auckland
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.
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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.
Camille Laibe 
