ArticleThe Journal of physiology2010
BK channels mediate a novel ionic mechanism that regulates glucose-dependent electrical activity and insulin secretion in mouse pancreatic β-cells.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Article
- The NMDAR-BK channelosomes as regulators of synaptic plasticity.Biochemical Society transactions · 2025Review
- Molecular mechanism responsible for sex differences in electrical activity of mouse pancreatic β cells.JCI insight · 2024Article
- All-potassium channel CRISPR screening reveals a lysine-specific pathway of insulin secretion.Molecular metabolism · 2024Article
- A Novel Peptide COXCurrent protein & peptide science · 2024Article
- The Dynamics of Calcium Signaling in Beta Cells-A Discussion on the Comparison of Experimental and Modelling Data.International journal of molecular sciences · 2023Article
- Article
- Celebrities in the heart, strangers in the pancreatic beta cell: Voltage-gated potassium channels KActa physiologica (Oxford, England) · 2022Review
- Beta-Cell Adaptation to Pregnancy - Role of Calcium Dynamics.Frontiers in endocrinology · 2022Review
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Neonatal Diabetes in Patients Affected by Liang-Wang Syndrome Carrying KCNMA1 Variant p.(Gly375Arg) Suggest a Potential Role of CaCurrent issues in molecular biology · 2021Article
- Regulatory effects of protein S-acylation on insulin secretion and insulin action.Open biology · 2021Review
- 'Resistance is futile?' - paradoxical inhibitory effects of KThe Journal of physiology · 2020Review
- From Local to Global Modeling for Characterizing Calcium Dynamics and Their Effects on Electrical Activity and Exocytosis in Excitable Cells.International journal of molecular sciences · 2019Article
- Review
- Oestrogen receptor β mediates the actions of bisphenol-A on ion channel expression in mouse pancreatic beta cells.Diabetologia · 2019Article
- A computational model of large conductance voltage and calcium activated potassium channels: implications for calcium dynamics and electrophysiology in detrusor smooth muscle cells.Journal of computational neuroscience · 2019Article
- Insulin Release Mechanism Modulated by Toxins Isolated from Animal Venoms: From Basic Research to Drug Development Prospects.Molecules (Basel, Switzerland) · 2019Review
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Concise Whole-Cell Modeling of BKBiophysical journal · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
BK channels are large unitary conductance K(+) channels cooperatively activated by intracellular calcium and membrane depolarisation. We show that BK channels regulate electrical activity in β-cells of mouse pancreatic islets exposed to elevated glucose. In 11.1 mM glucose, the non-peptidyl BK channel blocker paxilline increased the height of β-cell action potentials (APs) by 21 mV without affecting burst- or silent-period durations. In isolated β-cells, paxilline increased AP height by 16 mV without affecting resting membrane potential. In voltage clamp, paxilline blocked a transient component of outward current activated by a short depolarisation, which accounted for at least 90% of the initial outward K(+) current. This BK current (I(BK)) was blocked by the Ca(2+) channel blockers Cd(2+) (200 μM) or nimodipine (1 μM), and potentiated by FPL-64176 (1 μM). I(BK) was also 56% blocked by the BK channel blocker iberiotoxin (100 nM). I(BK) activated more than 10-fold faster than the delayed rectifier I(Kv) over the physiological voltage range, and partially inactivated. An AP-like command revealed that I(BK) activated and deactivated faster than I(Kv) and accounted for 86% of peak I(K), explaining why I(BK) block increased AP height. A higher amplitude AP-like command, patterned on an AP recorded in 11.1 mM glucose plus paxilline, activated 4-fold more I(Kv) and significantly increased Ca(2+) entry. Paxilline increased insulin secretion in islets exposed to 11.1 mM glucose by 67%, but did not affect basal secretion in 2.8 mM glucose. These data suggest a modified model of β-cell AP generation where I(BK) and I(Kv) coordinate the AP repolarisation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.