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Cited by 137Pancreatic function and diabetesIon channel regulation and functionCardiac electrophysiology and arrhythmias

Activation of Ca2+-Dependent K+ Channels Contributes to Rhythmic Firing of Action Potentials in Mouse Pancreatic β Cells

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Göpel, Sven O., Kanno, Takahiro, Barg, Sebastian, Eliasson, Lena, Galvanovskis, Juris, Renström, Erik, Rorsman, Patrik·1999·The Journal of General Physiology
DOI 10.1085/jgp.114.6.759PMC PMC2230648
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Abstract

We have applied the perforated patch whole-cell technique to β 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 Ca2+ influx but unaffected by apamin and charybdotoxin, two blockers of Ca2+-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 Ca2+-activated K+ current plays an important role in the generation of oscillatory electrical activity in the β cell.

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Crossref · 10.1085/jgp.114.6.759

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  • The existence of a KATP channel-independent component of Kslow (contributed by SK channels) might explain the paradox that slow waves persist in islets of SUR1 knockout mice, which lack functional KATP channels.

    “The existence of a KATP channel-independent component of Kslow (contributed by SK channels) might explain the paradox that slow waves persist in islets of SUR1 knockout mice, which lack functional KATP channels (157, 223).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [223]

    The Results (Pharmacology; page unavailable) report that Kslow was unaffected by the KATP-channel inhibitor tolbutamide. The Discussion (Function of the Kslow Current; page unavailable) identifies SK1 channels as a possible, not established, contributor. Our copy does not address SUR1-knockout mice or the persistence of slow waves in their islets. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • The reduced exocytotic capacity of β-cells in intact islets is not the consequence of reduced Ca2+ entry; if anything, the Ca2+ channel density is greater in β-cells in intact islets.

    “The reduced exocytotic capacity of β-cells in intact islets is likewise not the consequence of reduced Ca2+ entry: if anything, the Ca2+ channel density is greater in β-cells in intact islets (223).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [223]

    The Results (Relationship between Kslow Current Activation and [Ca2+]i; page unavailable) report that Ca2+ current was 40% smaller in dispersed β-cells than in β-cells within intact islets, supporting the comparison of Ca2+ entry. The Discussion reports cell capacitance but does not directly establish Ca2+ channel density. The paper does not assess reduced exocytotic capacity or test whether Ca2+ entry causes it. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Kslow is blocked by TEA with an IC50 of approximately 5 mM and by UCL1684.

    “It is also blocked by TEA with an IC50 of ~5 mM (223) and by UCL1684.”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [223]

  • Kslow likely contributes to the pacemaker current.

    “Thus Kslow likely contributes to the pacemaker current.”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [223]

  • The reduction of Kslow in dispersed β-cells may account for the loss of normal oscillatory electrical activity seen in this preparation.

    “which may account for the loss of normal oscillatory electrical activity seen in this preparation (but see (217)).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [223]

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Authors
Göpel, S. O., Kanno, T., Barg, S., Eliasson, L., Galvanovskis, J., Renström, E., & Rorsman, P.
Affiliations
Lund University (SE)
ORCID
Venue
The Journal of General Physiology
Publisher
Rockefeller University Press
Published
1999-11-15
Volume
114
Issue
6
Pages
759-770
ISSN
  • 0022-1295 (ISSN-L)
  • 1540-7748
DOI
10.1085/jgp.114.6.759
PMC
PMC2230648
OpenAlex
W2065171939
Cited by
137
References
40
Citations by year
2026: 1 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 1 · 2015: 7 · 2014: 10 · 2013: 7 · 2012: 5
FWCI
4.91
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of General Physiology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
calcium-activated potassium channels, pancreatic beta cells, pancreatic islets, tetraethylammonium, ATP-sensitive potassium channels, apamin, charybdotoxin, tolbutamide, potassium conductance, bursting oscillations
MeSH terms
Action Potentials, Animals, Electrophysiology, Hypoglycemic Agents, Islets of Langerhans, Membrane Potentials, Tolbutamide, Potassium Channels, Patch-Clamp Techniques, ATP-Binding Cassette Transporters, Potassium Channels, Inwardly Rectifying, Potassium Channels, Calcium-Activated, Potassium Channel Blockers, Large-Conductance Calcium-Activated Potassium Channels, Mice, KATP Channels, In Vitro Techniques

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