Oscillations of membrane potential and cytosolic Ca2+ concentration in SUR1−/− beta cells
Open accessAbstract
Aims/hypothesis SUR1(ABCC8)(-/-) mice lacking functional K(ATP) channels are an appropriate model to test the significance of K(ATP) channels in beta-cell function. We examined how this gene deletion interferes with stimulus-secretion coupling. We tested the influence of metabolic inhibition and galanin, whose mode of action is controversial. Methods Plasma membrane potential (Vm) and currents were measured with microelectrodes or the patch-clamp technique; cytosolic Ca(2+) concentrations ([Ca(2+)](c)) and mitochondrial membrane potential (DeltaPsi) were measured using fluorescent dyes. Results In contrast to the controls, SUR1(-/-) beta cells showed electrical activity even at a low glucose concentration. Continuous spike activity was measured with the patch-clamp technique, but with microelectrodes slow oscillations in Vm consisting of bursts of Ca(2+)-dependent action potentials were detected. [Ca(2+)](c) showed various patterns of oscillations or a sustained increase. Sodium azide did not hyperpolarize SUR1(-/-) beta cells. The depolarization of DeltaPsi evoked by sodium azide was significantly lower in SUR1(-/-) than SUR1(+/+) cells. Galanin transiently decreased action potential frequency and [Ca(2+)](c) in cells from both SUR1(-/-) and SUR1(+/+) mice. Conclusion/interpretation The strong dependence of Vm and [Ca(2+)](c) on glucose concentration observed in SUR1(+/+) beta cells is disrupted in the knock-out cells. This demonstrates that both parameters oscillate in the absence of functional K(ATP) channels. The lack of effect of metabolic inhibition by sodium azide shows that in SUR1(-/-) beta cells changes in ATP/ADP no longer link glucose metabolism and Vm. The results with galanin suggest that this peptide affects beta cells independently of K(ATP) currents and thus could contribute to the regulation of beta-cell function in SUR1(-/-) animals.
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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 [157]
The Results section reports slow membrane-potential oscillations in intact SUR1−/− islets despite the absence of functional KATP channels. The Discussion proposes a second oscillator and mentions a Ca2+-dependent K+ current in wild-type cells, but does not identify SK channels or show that an SK contribution to Kslow explains the knockout-islet oscillations. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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References 49 · Cited by 70
Research works printed but not linked: 1
- Smith PA, Ashcroft FM, Rorsman P (1990) Simultaneous recordings of glucose dependent electrical activity and ATP-regulated K + -currents in isolated mouse pancreatic β-cells. FEBS Letters 261:167-190
- Authors
- Düfer, M., Haspel, D., Krippeit-Drews, P., Aguilar-Bryan, L., Bryan, J., & Drews, G.
- Affiliations
- University of Tübingen (DE)
- Baylor College of Medicine (US)
- Corresponding author
- Drews, G.
- Venue
- Diabetologia
- Published
- 2004-03
- Volume
- 47
- Issue
- 3
- Pages
- 488-498
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2064770405
- Cited by
- 70
- References
- 49
- Citations by year
- 2026: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 2 · 2018: 5 · 2017: 8 · 2015: 3 · 2014: 6 · 2013: 3 · 2012: 2
- FWCI
- 5.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK52771, R01DK052771)
- 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
- SUR1, ABCC8, ATP-sensitive potassium channels, pancreatic beta cells, membrane potential oscillations, cytosolic calcium oscillations, stimulus-secretion coupling, galanin, mitochondrial membrane potential, sodium azide, glucose metabolism, beta-cell function
- MeSH terms
- Action Potentials, Animals, Calcium, Cytosol, Glucose, Islets of Langerhans, Kinetics, Membrane Potentials, Mice, Inbred C57BL, Receptors, Drug, Mice, Knockout, ATP-Binding Cassette Transporters, Potassium Channels, Inwardly Rectifying, Multidrug Resistance-Associated Proteins, ATP-Binding Cassette, Sub-Family C Proteins, Mice, Sulfonylurea Receptors
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