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Cited by 177Ion channel regulation and functionPancreatic function and diabetesIon Channels and Receptors

Properties and calcium‐dependent inactivation of calcium currents in cultured mouse pancreatic B‐cells.

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Plant, T D·1988·The Journal of Physiology
DOI 10.1113/jphysiol.1988.sp017316PMC PMC1190852
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Abstract

1. Ca2+ currents were recorded using the whole‐cell mode of the patch‐clamp technique from mouse pancreatic B‐cells kept in culture for 1‐4 days. B‐cells were identified in the cell‐attached mode by their response to a change in the glucose concentration from 3 to 15 or 20 mM or by their inward currents. 2. Only one component of Ca2+ current was observed in these cells, which activated at potentials greater than ‐50 mV and was blocked by nitrendipine (5 microM), and increased in amplitude by CGP 28392 (5 microM). 3. During maintained depolarizations the Ca2+ current inactivated considerably but not completely. Inactivation was most marked at potentials where the Ca2+ currents were large, but in general was slower for currents at potentials greater than 0 mV than at more negative potentials. 4. Two‐pulse experiments showed that the inactivation curve for the Ca2+ current was U‐shaped, returning to unity at potentials approaching the Ca2+ equilibrium potential. Measurements of Ca2+ entry showed that inactivation was dependent on the amount of Ca2+ entering during the pre‐pulse, independent of the pre‐pulse potential. 5. Ca2+ currents were not appreciably slowed when BAPTA, a faster buffer of Ca2+, replaced EGTA in the pipette solution. 6. Replacement of Ca2+ in the external solution by Ba2+ increased the amplitude of the inward current and largely abolished inactivation. Large inward currents through Ca2+ channels were observed in the absence of divalent cations in the external solution (+EGTA), which were presumably carried by Na+. These currents did not inactivate during 150 ms depolarizations, but were increased in amplitude by CGP 28392 (5 microM) and blocked by D600 (30 microM). 7. The observations suggest that normal mouse pancreatic B‐cells have only one type of Ca2+ channel which is dihydropyridine sensitive and inactivates by a mechanism which is almost purely Ca2+ dependent. Inactivation of the Ca2+ current will probably be important in the control of Ca2+ entry during glucose‐induced electrical activity.

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  • During membrane depolarization, β-cell Ca2+ currents undergo both Ca2+- and voltage-dependent inactivation.

    “During membrane depolarization, β-cell Ca2+ currents undergo both Ca2+- and voltage-dependent inactivation (515).”

    From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [515]

    The paper’s summary (points 4 and 7; page not supplied) says inactivation depended on the amount of Ca2+ entering, independently of pre-pulse potential. It describes the mechanism as almost purely Ca2+-dependent, contrary to the claim that voltage-dependent inactivation also occurs. (LLM, conf=0.88)

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Authors
Plant, T. D.
Affiliations
Saarland University (DE)
Corresponding author
Plant, T D
ORCID
Plant, T D
Venue
The Journal of Physiology
Publisher
Wiley
Published
1988-10
Volume
404
Issue
1
Pages
731-747
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.1988.sp017316
PMC
PMC1190852
OpenAlex
W1990572888
Cited by
177
References
0
Citations by year
2026: 1 · 2022: 1 · 2021: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 5 · 2012: 4
FWCI
5.50
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords
calcium current, pancreatic beta cells, calcium channel inactivation, calcium-dependent inactivation, dihydropyridine-sensitive channels, L-type calcium channels, nitrendipine, barium substitution, calcium buffering, BAPTA, EGTA, calcium influx
MeSH terms
Action Potentials, Animals, Barium, Calcium, Calcium Channel Blockers, Cells, Cultured, Egtazic Acid, Islets of Langerhans, Membrane Potentials, Nitrendipine, Pyridines, Sodium, Time Factors, Calcium Channels, Mice

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