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Electrophysiology of pancreatic beta-cells in intact mouse islets of Langerhans

Rorsman, Patrik; Eliasson, Lena LU ; Kanno, Takahiro; Zhang, Quan and Gopel, Sven (2011) In Progress in Biophysics and Molecular Biology 107(2). p.224-235
Abstract
When exposed to intermediate glucose concentrations (6-16 mol/l), pancreatic beta-cells in intact islets generate bursts of action potentials (superimposed on depolarised plateaux) separated by repolarised electrically silent intervals. First described more than 40 years ago, these oscillations have continued to intrigue beta-cell electrophysiologists. To date, most studies of beta-cell ion channels have been performed on isolated cells maintained in tissue culture (that do not burst). Here we will review the electrophysiological properties of beta-cells in intact, freshly isolated, mouse pancreatic islets. We will consider the role of ATP-regulated K+-channels (K-ATP-channels), small-conductance Ca2+-activated K+-channels and... (More)
When exposed to intermediate glucose concentrations (6-16 mol/l), pancreatic beta-cells in intact islets generate bursts of action potentials (superimposed on depolarised plateaux) separated by repolarised electrically silent intervals. First described more than 40 years ago, these oscillations have continued to intrigue beta-cell electrophysiologists. To date, most studies of beta-cell ion channels have been performed on isolated cells maintained in tissue culture (that do not burst). Here we will review the electrophysiological properties of beta-cells in intact, freshly isolated, mouse pancreatic islets. We will consider the role of ATP-regulated K+-channels (K-ATP-channels), small-conductance Ca2+-activated K+-channels and voltage-gated Ca2+-channels in the generation of the bursts. Our data indicate that K-ATP-channels not only constitute the glucose-regulated resting conductance in the beta-cell but also provide a variable K+- conductance that influence the duration of the bursts of action potentials and the silent intervals. We show that inactivation of the voltage-gated Ca2+-current is negligible at voltages corresponding to the plateau potential and consequently unlikely to play a major role in the termination of the burst. Finally, we propose a model for glucose-induced beta-cell electrical activity based on observations made in intact pancreatic islets. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Pancreas, Beta-cell, Insulin, Ion channels, Glucose, Electrical activity
in
Progress in Biophysics and Molecular Biology
volume
107
issue
2
pages
224 - 235
publisher
Elsevier
external identifiers
  • wos:000297489800003
  • scopus:82455205940
ISSN
1873-1732
DOI
10.1016/j.pbiomolbio.2011.06.009
language
English
LU publication?
yes
id
deb7b0ee-40e3-4cef-9a07-31cccd71b2c6 (old id 2279409)
date added to LUP
2012-01-11 15:35:34
date last changed
2017-10-01 03:30:53
@article{deb7b0ee-40e3-4cef-9a07-31cccd71b2c6,
  abstract     = {When exposed to intermediate glucose concentrations (6-16 mol/l), pancreatic beta-cells in intact islets generate bursts of action potentials (superimposed on depolarised plateaux) separated by repolarised electrically silent intervals. First described more than 40 years ago, these oscillations have continued to intrigue beta-cell electrophysiologists. To date, most studies of beta-cell ion channels have been performed on isolated cells maintained in tissue culture (that do not burst). Here we will review the electrophysiological properties of beta-cells in intact, freshly isolated, mouse pancreatic islets. We will consider the role of ATP-regulated K+-channels (K-ATP-channels), small-conductance Ca2+-activated K+-channels and voltage-gated Ca2+-channels in the generation of the bursts. Our data indicate that K-ATP-channels not only constitute the glucose-regulated resting conductance in the beta-cell but also provide a variable K+- conductance that influence the duration of the bursts of action potentials and the silent intervals. We show that inactivation of the voltage-gated Ca2+-current is negligible at voltages corresponding to the plateau potential and consequently unlikely to play a major role in the termination of the burst. Finally, we propose a model for glucose-induced beta-cell electrical activity based on observations made in intact pancreatic islets. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.},
  author       = {Rorsman, Patrik and Eliasson, Lena and Kanno, Takahiro and Zhang, Quan and Gopel, Sven},
  issn         = {1873-1732},
  keyword      = {Pancreas,Beta-cell,Insulin,Ion channels,Glucose,Electrical activity},
  language     = {eng},
  number       = {2},
  pages        = {224--235},
  publisher    = {Elsevier},
  series       = {Progress in Biophysics and Molecular Biology},
  title        = {Electrophysiology of pancreatic beta-cells in intact mouse islets of Langerhans},
  url          = {http://dx.doi.org/10.1016/j.pbiomolbio.2011.06.009},
  volume       = {107},
  year         = {2011},
}