Delayed rectifying and calcium-activated K+ channels and their significance for action potential repolarization in mouse pancreatic beta-cells.
Open accessAbstract
The contribution of Ca2(+)-activated and delayed rectifying K+ channels to the voltage-dependent outward current involved in spike repolarization in mouse pancreatic beta-cells (Rorsman, P., and G. Trube. 1986. J. Physiol. 374:531-550) was assessed using patch-clamp techniques. A Ca2(+)-dependent component could be identified by its rapid inactivation and sensitivity to the Ca2+ channel blocker Cd2+. This current showed the same voltage dependence as the voltage-activated (Cd2(+)-sensitive) Ca2+ current and contributed 10-20% to the total beta-cell delayed outward current. The single-channel events underlying the Ca2(+)-activated component were investigated in cell-attached patches. Increase of [Ca2+]i invariably induced a dramatic increase in the open state probability of a Ca2(+)-activated K+ channel. This channel had a single-channel conductance of 70 pS [( K+]o = 5.6 mM). The Ca2(+)-independent outward current (constituting greater than 80% of the total) reflected the activation of an 8 pS [( K+]o = 5.6 mM; [K+]i = 155 mM) K+ channel. This channel was the only type observed to be associated with action potentials in cell-attached patches. It is suggested that in mouse beta-cells spike repolarization results mainly from the opening of the 8-pS delayed rectifying K+ channel.
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The single-channel conductance of BK channels is 70-90 pS for outward currents recorded in cell-attached patches with physiological K+ gradients and 240 pS for inward currents recorded in excised inside-out patches exposed to symmetrical 140 mM K+.
“The single-channel conductance is 70-90 pS for outward currents recorded in cell-attached patches when measured using physiological K+ gradients (632) and 240 pS for inward currents recorded in excised inside-out patches exposed to symmetrical 140 mM K+ (128).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [632]
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Experimental — accuracy not yet measuredBK channels contribute little to either glucose-induced membrane depolarization or action potential repolarization in β-cells.
“it was concluded that BK channels contribute little to either glucose-induced membrane depolarization or action potential repolarization in β-cells.”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [632]
In the Discussion (p. 1057), the paper says the calcium-activated K+ current is not critical for action-potential repolarization and that blocking its channel has little effect on glucose-induced electrical activity in mouse β-cells. It does not specifically establish that the channel contributes little to glucose-induced membrane depolarization, and the claim omits the mouse-cell qualifier. (LLM, conf=0.83)
Experimental — accuracy not yet measuredCharybdotoxin, a blocker of BK channels, did not affect electrical activity, action potential firing, or the voltage-gated K+ current of mouse β-cells.
“However, following the discovery of the central role of the KATP channel in glucose-dependent depolarization, and the finding that charybdotoxin, a blocker of BK channels, did not affect electrical activity, action potential firing (356), or the voltage-gated K+ current of mouse β-cells (632), it was concluded that BK channels contribute little to either glucose-induced membrane depolarization or”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [632]
The paper reports that calcium-activated K+ current accounts for 10–20% of the delayed outward current (p. 1048), but that does not establish the effect of charybdotoxin. A search of our copy for charybdotoxin and toxin sensitivity found no passage testing whether it affects mouse β-cell electrical activity, action-potential firing, or voltage-gated K+ current. (LLM, conf=0.74)
Experimental — accuracy not yet measured
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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
Self-citationVoltage‐gated and resting membrane currents recorded from B‐cells in intact mouse pancreatic islets
Göpel, S., Kanno, T., Barg, S., Galvanovskis, J., & Rorsman, P. (1999) · The Journal of Physiology · doi:10.1111/j.1469-7793.1999.00717.x · Cited by 226 · see citing works
Self-citation
- Authors
- Smith, P. A., Bokvist, K., Arkhammar, P., Berggren, P. O., & Rorsman, P.
- Affiliations
- University of Gothenburg (SE)
- Venue
- The Journal of general physiology
- Publisher
- Rockefeller University Press
- Published
- 1990-06-01
- Volume
- 95
- Issue
- 6
- Pages
- 1041-1059
- ISSN
- 0022-1295 (ISSN-L)
- 1540-7748
- PMC
- PMC2216351
- OpenAlex
- W2118602922
- Cited by
- 86
- References
- 0
- Citations by year
- 2026: 1 · 2024: 2 · 2023: 1 · 2021: 3 · 2020: 1 · 2019: 3 · 2017: 3 · 2016: 1 · 2014: 4 · 2013: 3 · 2012: 6
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of General Physiology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- 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
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- calcium-activated potassium channels, action potential repolarization, pancreatic beta cells, outward potassium current, cadmium block, single-channel conductance, open probability, intracellular calcium, voltage-gated potassium channels
- MeSH terms
- Insulin Secretion, Action Potentials, Animals, Calcium, Calcium Channel Blockers, Cations, Divalent, Insulin, Islets of Langerhans, Potassium, Potassium Channels, Mice, In Vitro Techniques
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