Muscarinic receptor modulation of glucose‐induced electrical activity in mouse pancreatic B‐cells
Open accessAbstract
Acetylcholine (1–10 μM) depolarized the membrane and stimulated glucose‐induced bursts of electrical activity in mouse pancreatic B‐cells. The acetylcholine effects were mimicked by muscarine while nicotine had no effect on membrane potential. Pirenzepine, an antagonist of the classical M1‐type muscarinic receptors, but not gallamine (1–100 μM), an antagonist of the classical M2‐type receptors, antagonized the acetylcholine action on glucose‐induced electrical activity (IC 50 = 0.25 μM). Bethanechol, an agonist of the classical M2‐type muscarinic receptors, was approximately 100 times less effective than acetylcholine in stimulating the electrical activity. In addition, acetylcholine (1 μM) induced a marked increase (25%) in input resistance to the B‐cell membrane. The results indicate that acetylcholine exerted its effects on the B‐cell membrane by inhibiting K+ conductance via activation of a muscarinic receptor subtype distinct from the classical M2‐type receptor.
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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 [590]
The electrical-activity results (page not specified) report that ACh transiently increased spike frequency and sustained a higher burst frequency while present. They also describe silent phases between bursts, rather than a membrane locked at a plateau potential; that part of the claim is not supported. (LLM, conf=0.88)
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Cites
Effects of Adrenergic and Cholinergic Agents Upon Insulin Secretion<i>in Vitro</i>
MALAISSE, W., MALAISSE-LAGAE, F., WRIGHT, P. H., & ASHMORE, J. (1967) · Endocrinology · doi:10.1210/endo-80-5-975 · Cited by 258 · see citing works
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Research works printed but not linked: 2
- Egan, T.M. and North, R.A. (1984) Proc. IX Int. Congr. Pharmacol., 324 pp.
- Atwater, I., Carroll, P. and Li, M.X. (1988) in: Molecular and Cellular Biology of Diabetes Mellitus, vol.l, pp.49-68, Alan R. Liss, New York.
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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
- Santos, R. M., & Rojas, E.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Santos, Rosa M.
- ORCID
- Santos, Rosa M.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 1989-06-05
- Volume
- 249
- Issue
- 2
- Pages
- 411-417
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2039021913
- Cited by
- 23
- References
- 1
- Citations by year
- 2018: 1 · 2017: 1
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- muscarinic receptors, acetylcholine, pancreatic beta cells, M1 muscarinic receptor, M2 muscarinic receptor, pirenzepine, gallamine, bethanechol, membrane depolarization, potassium conductance, input resistance, insulin secretion
- MeSH terms
- Acetylcholine, Animals, Bethanechol Compounds, Cells, Cultured, Glucose, Membrane Potentials, Muscarine, Pancreas, Pirenzepine, Receptors, Muscarinic, Bethanechol, Mice, In Vitro Techniques
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