Activation of Ca(2+)-dependent K(+) channels contributes to rhythmic firing of action potentials in mouse pancreatic beta cells
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1114673
- author
- Göpel, Sven LU ; Kanno, Takahiro ; Barg, Sebastian LU ; Eliasson, Lena LU ; Galvanovskis, Juris LU ; Renström, Erik LU and Rorsman, Patrik LU
- organization
- publishing date
- 1999
- 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 (<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.}}, 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}}, }