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Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells

Göpel, Sven LU ; Kanno, Takahiro ; Barg, Sebastian LU ; Eliasson, Lena LU orcid ; Galvanovskis, Juris LU ; Renström, Erik LU and Rorsman, Patrik LU (1999) In Journal of General Physiology 114(6). p.759-770
Abstract
We have applied the perforated patch whole-cell technique to beta cells within intact pancreatic islets to identify the current underlying the glucose-induced rhythmic firing of action potentials. Trains of depolarizations (to simulate glucose-induced electrical activity) resulted in the gradual (time constant: 2.3 s) development of a small (<0.8 nS) K(+) conductance. The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) channels, and was insensitive to tolbutamide (a blocker of ATP-regulated K(+) channels) but partially (>60%) blocked by high (10-20 mM) concentrations of tetraethylammonium. Upon cessation of electrical stimulation, the current deactivated... (More)
We have applied the perforated patch whole-cell technique to beta cells within intact pancreatic islets to identify the current underlying the glucose-induced rhythmic firing of action potentials. Trains of depolarizations (to simulate glucose-induced electrical activity) resulted in the gradual (time constant: 2.3 s) development of a small (<0.8 nS) K(+) conductance. The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) channels, and was insensitive to tolbutamide (a blocker of ATP-regulated K(+) channels) but partially (>60%) blocked by high (10-20 mM) concentrations of tetraethylammonium. Upon cessation of electrical stimulation, the current deactivated exponentially with a time constant of 6.5 s. This is similar to the interval between two successive bursts of action potentials. We propose that this Ca(2+)-activated K(+) current plays an important role in the generation of oscillatory electrical activity in the beta cell. (Less)
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author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Ca2+-activated K+ channel, pancreas, insulin, Ca2+, membrane potential
in
Journal of General Physiology
volume
114
issue
6
pages
759 - 770
publisher
Rockefeller Institute for Medical Research
external identifiers
  • pmid:10578013
  • scopus:0344339740
ISSN
0022-1295
language
English
LU publication?
yes
id
ff0d3911-665e-49de-ab89-e6c91157a3da (old id 1114673)
alternative location
http://www.jgp.org/cgi/content/full/114/6/759
date added to LUP
2016-04-01 16:11:30
date last changed
2022-04-30 19:31:18
@article{ff0d3911-665e-49de-ab89-e6c91157a3da,
  abstract     = {{We have applied the perforated patch whole-cell technique to beta cells within intact pancreatic islets to identify the current underlying the glucose-induced rhythmic firing of action potentials. Trains of depolarizations (to simulate glucose-induced electrical activity) resulted in the gradual (time constant: 2.3 s) development of a small (&lt;0.8 nS) K(+) conductance. The current was dependent on Ca(2+) influx but unaffected by apamin and charybdotoxin, two blockers of Ca(2+)-activated K(+) channels, and was insensitive to tolbutamide (a blocker of ATP-regulated K(+) channels) but partially (&gt;60%) blocked by high (10-20 mM) concentrations of tetraethylammonium. Upon cessation of electrical stimulation, the current deactivated exponentially with a time constant of 6.5 s. This is similar to the interval between two successive bursts of action potentials. We propose that this Ca(2+)-activated K(+) current plays an important role in the generation of oscillatory electrical activity in the beta cell.}},
  author       = {{Göpel, Sven and Kanno, Takahiro and Barg, Sebastian and Eliasson, Lena and Galvanovskis, Juris and Renström, Erik and Rorsman, Patrik}},
  issn         = {{0022-1295}},
  keywords     = {{Ca2+-activated K+ channel; pancreas; insulin; Ca2+; membrane potential}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{759--770}},
  publisher    = {{Rockefeller Institute for Medical Research}},
  series       = {{Journal of General Physiology}},
  title        = {{Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells}},
  url          = {{http://www.jgp.org/cgi/content/full/114/6/759}},
  volume       = {{114}},
  year         = {{1999}},
}