ArticleBiophysical journal2009
A model of action potentials and fast Ca2+ dynamics in pancreatic beta-cells.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Ultrafast multicellular calcium imaging of calcium spikes in mouse beta cells in tissue slices.Acta physiologica (Oxford, England) · 2025Article
- Model of Calcium Dynamics RegulatingActa biotheoretica · 2024Article
- Deconstructing the integrated oscillator model for pancreatic β-cells.Mathematical biosciences · 2023Article
- A complete biomechanical model ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Oscillations in K(ATP) conductance drive slow calcium oscillations in pancreatic β-cells.Biophysical journal · 2022Article
- A sodium background conductance controls the spiking pattern of mouse adrenal chromaffin cells in situ.The Journal of physiology · 2021Article
- GPCR mediated control of calcium dynamics: A systems perspective.Cellular signalling · 2020Review
- Pancreatic Beta Cell G-Protein Coupled Receptors and Second Messenger Interactions: A Systems Biology Computational Analysis.PloS one · 2016Article
- Modeling K,ATP--dependent excitability in pancreatic islets.Biophysical journal · 2014Article
- Mathematical models of electrical activity of the pancreatic β-cell: a physiological review.Islets · 2014Review
- Direct measurements of oscillatory glycolysis in pancreatic islet β-cells using novel fluorescence resonance energy transfer (FRET) biosensors for pyruvate kinase M2 activity.The Journal of biological chemistry · 2013Article
- Article
- Buffering capacity explains signal variation in symbiotic calcium oscillations.Plant physiology · 2012Article
- Coupling of metabolic, second messenger pathways and insulin granule dynamics in pancreatic beta-cells: a computational analysis.Progress in biophysics and molecular biology · 2011Review
- Ionic mechanisms and Ca2+ dynamics underlying the glucose response of pancreatic β cells: a simulation study.The Journal of general physiology · 2011Article
- A biophysical model of electrical activity in human β-cells.Biophysical journal · 2010Article
- Bursting and calcium oscillations in pancreatic beta-cells: specific pacemakers for specific mechanisms.American journal of physiology. Endocrinology and metabolism · 2010Review
- Use of virtual cell in studies of cellular dynamics.International review of cell and molecular biology · 2010Review
- Article
- Ion channels and regulation of insulin secretion in human β-cells: a computational systems analysis.IsletsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We examined the ionic mechanisms mediating depolarization-induced spike activity in pancreatic beta-cells. We formulated a Hodgkin-Huxley-type ionic model for the action potential (AP) in these cells based on voltage- and current-clamp results together with measurements of Ca(2+) dynamics in wild-type and Kv2.1 null mouse islets. The model contains an L-type Ca(2+) current, a "rapid" delayed-rectifier K(+) current, a small slowly-activated K(+) current, a Ca(2+)-activated K(+) current, an ATP-sensitive K(+) current, a plasma membrane calcium-pump current and a Na(+) background current. This model, coupled with an equation describing intracellular Ca(2+) homeostasis, replicates beta-cell AP and Ca(2+) changes during one glucose-induced spontaneous spike, the effects of blocking K(+) currents with different inhibitors, and specific complex spike in mouse islets lacking Kv2.1 channels. The currents with voltage-independent gating variables can also be responsible for burst behavior. Original features of this model include new equations for L-type Ca(2+) current, assessment of the role of rapid delayed-rectifier K(+) current, and Ca(2+)-activated K(+) currents, demonstrating the important roles of the Ca(2+)-pump and background currents in the APs and bursts. This model provides acceptable fits to voltage-clamp, AP, and Ca(2+) concentration data based on in silico analysis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.