ArticleThe Journal of membrane biology1991
Charybdotoxin-sensitive K(Ca) channel is not involved in glucose-induced electrical activity in pancreatic beta-cells.
Article in The Journal of membrane biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.Physiological reviews · 2018Review
- Review
- Mathematical models of electrical activity of the pancreatic β-cell: a physiological review.Islets · 2014Review
- Ionic mechanisms and Ca2+ dynamics underlying the glucose response of pancreatic β cells: a simulation study.The Journal of general physiology · 2011Article
- BK channels affect glucose homeostasis and cell viability of murine pancreatic beta cells.Diabetologia · 2011Article
- BK channels mediate a novel ionic mechanism that regulates glucose-dependent electrical activity and insulin secretion in mouse pancreatic β-cells.The Journal of physiology · 2010Article
- Article
- Action potentials and insulin secretion: new insights into the role of Kv channels.Diabetes, obesity & metabolism · 2007Article
- The electrophysiology of the beta-cell based on single transmembrane protein characteristics.Biophysical journal · 2007Article
- Kv2.1 ablation alters glucose-induced islet electrical activity, enhancing insulin secretion.Cell metabolism · 2007Article
- Effects of I(Ks) channel inhibitors in insulin-secreting INS-1 cells.Pflugers Archiv : European journal of physiology · 2005Article
- Pharmacological properties and functional role of Kslow current in mouse pancreatic beta-cells: SK channels contribute to Kslow tail current and modulate insulin secretion.The Journal of general physiology · 2005Article
- Voltage-dependent K(+) channels in pancreatic beta cells: role, regulation and potential as therapeutic targets.Diabetologia · 2003Review
- Calcium-activated K+ channels of mouse beta-cells are controlled by both store and cytoplasmic Ca2+: experimental and theoretical studies.The Journal of general physiology · 2002Article
- Effect of Na/Ca exchange on plateau fraction and [Ca]i in models for bursting in pancreatic beta-cells.Biophysical journal · 1999Article
- Characterization of a Ca2+-activated K+ current in insulin-secreting murine betaTC-3 cells.The Journal of physiology · 1998Article
- Article
- Characterization of the G protein coupling of SRIF and beta-adrenergic receptors to the maxi KCa channel in insulin-secreting cells.The Journal of membrane biology · 1995Article
- Ionic mechanisms involved in the regulation of insulin secretion by muscarinic agonists.The Journal of membrane biology · 1995Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of charybdotoxin (CTX) on single [Ca2+]-activated potassium channel (K(Ca)) activity and whole-cell K+ currents were examined in rat and mouse pancreatic beta-cells in culture using the patch-clamp method. The effects of CTX on glucose-induced electrical activity from both cultured beta-cells and beta-cells in intact islets were compared. K(Ca) activity was very infrequent at negative patch potentials (-70 less than Vm less than 0 mV), channel activity appearing at highly depolarized Vm. K(Ca) open probability at these depolarized Vm values was insensitive to glucose (10 and 20 mM) and the metabolic uncoupler 2,4 dinitrophenol (DNP). However, DNP blocked glucose-evoked action potential firing and reversed glucose-induced inhibition of the activity of K+ channels of smaller conductance. The venom from Leiurus quinquestriatus hebreus (LQV) and highly purified CTX inhibited K(Ca) channel activity when applied to the outer aspect of the excised membrane patch. CTX (5.8 and 18 nM) inhibited channel activity by 50 and 100%, respectively. Whole-cell outward K+ currents exhibited an early transient component which was blocked by CTX, and a delayed component which was insensitive to the toxin. The individual spikes evoked by glucose, recorded in the perforated-patch modality, were not affected by CTX (20 nM). Moreover, the frequency of slow oscillations in membrane potential, the frequency of action potentials and the rate of repolarization of the action potentials recorded from pancreatic islet beta-cells in the presence of glucose were not affected by CTX. We conclude that the K(Ca) does not participate in the steady-state glucose-induced electrical activity in rodent pancreatic islets.
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