Modulation of the Effect of Acetylcholine on Insulin Release by the Membrane Potential of B Cells*
Abstract
Mouse islets were used to test the hypothesis that the B cell membrane must be depolarized for acetylcholine to increase insulin release. The resting membrane potential of B cells (at 3 mM glucose) was slightly decreased (5 mV) by acetylcholine, but no electrical activity appeared. This depolarization was accompanied by a Ca-independent acceleration of 86Rb and 45Ca efflux but no insulin release. When the B cell membrane was depolarized by a stimulatory concentration of glucose (10 mM), acetylcholine potentiated electrical activity, accelerated 86Rb and 45Ca efflux, and increased insulin release. This latter effect, but not the acceleration of 45Ca efflux, was totally dependent on extracellular Ca. If glucose-induced depolarization of the B cell membrane was prevented by diazoxide, acetylcholine lost all effects but those produced at low glucose. In contrast, when the B cell membrane was depolarized by leucine or tolbutamide (at 3 mM glucose), acetylcholine triggered a further depolarization with appearance of electrical activity, accelerated 86Rb and 45Ca efflux, and stimulated insulin release. Acetylcholine produced similar effects (except for electrical activity) in the presence of high K or arginine which, unlike the above test agents, depolarize the B cell membrane by a mechanism other than a decrease in K+ permeability. Omission of extracellular Ca abolished the releasing effect of acetylcholine under all conditions but only partially decreased the stimulation of 45Ca e…
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ACh increases action potential firing and locks the membrane at the plateau potential.
“This increases action potential firing and ‘locks’ the membrane at the ‘plateau’ potential, from which action potentials are generated (277, 590).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [277]
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Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men
Rorsman, P., & Ashcroft, F. M. (2018) · Physiological Reviews · doi:10.1152/physrev.00008.2017 · Cited by 793 · see citing works
- Authors
- HERMANS, M. P., SCHMEER, W., & HENQUIN, J. C.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1987-05
- Volume
- 120
- Issue
- 5
- Pages
- 1765-1773
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2045986704
- Cited by
- 48
- References
- 0
- Citations by year
- 2025: 1 · 2024: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2017: 1 · 2013: 1
- FWCI
- 5.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- acetylcholine, insulin secretion, resting membrane potential, calcium efflux, potassium efflux, extracellular calcium, diazoxide, tolbutamide, leucine, L-arginine, glucose, calcium channels, electrical activity, pancreatic islets
- MeSH terms
- Insulin Secretion, Acetylcholine, Animals, Arginine, Calcium Radioisotopes, Cell Membrane, Diazoxide, Female, Glucose, Insulin, Islets of Langerhans, Leucine, Membrane Potentials, Potassium, Radioisotopes, Rubidium, Tolbutamide, Mice
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