The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Electrophysiology of Islet Cells
Abstract
Stimulus-Secretion Coupling (SSC) of pancreatic islet cells comprises electrical activity. Changes of the membrane potential (V(m)) are regulated by metabolism-dependent alterations in ion channel activity. This coupling is best explored in beta-cells. The effect of glucose is directly linked to mitochondrial metabolism as the ATP/ADP ratio determines the open probability of ATP-sensitive K(+) channels (K(ATP) channels). Nucleotide sensitivity and concentration in the direct vicinity of the channels are controlled by several factors including phospholipids, fatty acids, and kinases, e.g., creatine and adenylate kinase. Closure of K(ATP) channels leads to depolarization of beta-cells via a yet unknown depolarizing current. Ca(2+) influx during action potentials (APs) results in an increase of the cytosolic Ca(2+) concentration ([Ca(2+)](c)) that triggers exocytosis. APs are elicited by the opening of voltage-dependent Na(+) and/or Ca(2+) channels and repolarized by voltage- and/or Ca(2+)-dependent K(+) channels. At a constant stimulatory glucose concentration APs are clustered in bursts that are interrupted by hyperpolarized interburst phases. Bursting electrical activity induces parallel fluctuations in [Ca(2+)](c) and insulin secretion. Bursts are terminated by I(Kslow) consisting of currents through Ca(2+)-dependent K(+) channels and K(ATP) channels. This review focuses on structure, characteristics, physiological function, and regulation of ion channels in beta-cells. Info…
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“At 10 mM glucose, the active and silent phases last 5-10 s and 10-20 s, respectively and there are 2-4 bursts/min (154, 273, 570).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [154]
In the citing paper
“A number of hormones and neurotransmitters (e.g. somatostatin and adrenaline) transiently repolarise the β-cell and inhibit action potential firing and insulin secretion (154, 543).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [154]
In the citing paper
“Increasing glucose concentrations produce a progressive increase in burst duration at the expense of the repolarized intervals until firing finally becomes continuous, usually above ~20 mM glucose (154, 273).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [154]
Citations
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“Electrophysiological Characteristics The first measurements of single beta cell KATP channel currents were performed in 1984 by Cook and Hales (Cook and Hales 1984) in inside/outside patches where they could show the inhibition by cytosolic ATP.”
BackgroundMethodGloyn, A. L., Pearson, E. R., Antcliff, J. F., Proks, P., Bruining, G. J., Slingerland, A. S., Howard, N., Srinivasan, S., Silva, J. M. C. L., Molnes, J., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa032922 · Cited by 1,137
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Minimal model for membrane oscillations in the pancreatic beta-cell
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“The existence of BK channels in pancreatic beta cells and insulin-secreting cell lines has been verified by several groups (Braun et al. 2008; MacDonald et al. 2002a; Ribalet et al. 1988; Satin et al. 1989; Kukuljan et al. 1991; D€ufer et al. 2011).”
BackgroundInfluentialTransient receptor potential M3 channels are ionotropic steroid receptors in pancreatic β cells
Wagner, T. F. J., Loch, S., Lambert, S., Straub, I., Mannebach, S., Mathar, I., Düfer, M., Lis, A., Flockerzi, V., Philipp, S. E., et al. (2008) · Nature Cell Biology · doi:10.1038/ncb1801 · Cited by 392
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Chaffey, J. R., Young, J., Leslie, K., Partridge, K. M., Akhbari, P., Dhayal, S., Hill, J. L., Wedgwood, K. C. A., Burnett, E. C., Russell, M., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-94878-y · Cited by 6
Calamita, G., Delporte, C., & Marinelli, R. (2018) · Aquaporins in Health and Disease · doi:10.1201/b19017-12 · Cited by 6
Félix-Martínez, G. J., & Godínez-Fernández, J. R. (2015) · Mathematical Biosciences · doi:10.1016/j.mbs.2015.09.009 · Cited by 6
Role of KATP channels in β‐cell resistance to oxidative stress
Drews, G., & Düfer, M. (2012) · Diabetes, obesity and metabolism · doi:10.1111/j.1463-1326.2012.01644.x · Cited by 6
“During activation of the triggering pathway electrical activity is induced as soon as the threshold potential for the opening of voltage-dependent Ca2+ (and, depending on the species, Na+ channels) is attained [9].”
BackgroundInfluentialSelf-citationPan, C., Liu, Y., Wang, L., Fan, W.-Y., Ni, Y., Zhang, X., Wu, D., Li, C., Li, J., Li, Z., et al. (2024) · bioRxiv · doi:10.1101/2024.03.11.584397 · Cited by 5
“2 via EP2/EP4 signaling pathway.”
Zhao, X., Deng, L.-M., Ren, L., Yang, H., Wang, B., Zhu, X., Zhang, X.-L., Guo, C., Zhang, Y., & Liu, Y.-F. (2023) · Experimental Cell Research · doi:10.1016/j.yexcr.2023.113471 · Cited by 5
Microelectrode Array based Functional Testing of Pancreatic Islet Cells
Alassaf, A., Ishahak, M., Bowles, A. C., & Agarwal, A. (2020) · Micromachines · doi:10.3390/mi11050507 · Cited by 5
“Pancreatic β cells show oscillatory electrical activity known as slow waves in response to glucose [5,17].”
BackgroundNakayama, K., Tanabe, Y., Obara, K., & Ishikawa, T. (2012) · Springer eBooks · doi:10.1007/978-94-007-5073-9_14 · Cited by 4
Harvey, K. E., Tang, S., LaVigne, E. K., Pratt, E. P. S., & Hockerman, G. H. (2023) · PLoS ONE · doi:10.1371/journal.pone.0285316 · Cited by 4
“As the membrane potential is depolarized, Ca v channels are activated, leading to the upstroke of the action potential, followed by activation of K v channels which repolarize the membrane potential [64].”
Bai, T., Yang, H., Wang, H., Zhi, L., Liu, T., Cui, L.-J., Liu, W., Wang, Y., Zhang, M., Liu, Y.-F., et al. (2020) · Food & Function · doi:10.1039/d0fo01891k · Cited by 4
Ernsberger, U. (2015) · Cell and Tissue Research · doi:10.1007/s00441-015-2187-7 · Cited by 4
Pancreatic β Cells in Metabolic Syndrome
Hiriart, M., Velasco, M., Díaz‐García, C. M., Larqué, C., Sánchez-Soto, C., Albarado-Ibáñez, A., Chávez‐Maldonado, J. P., Toledo, A., & García-Delgado, N. (2014) · Springer eBooks · doi:10.1007/978-94-007-6686-0_27 · Cited by 3
The Role of TRP Channels in the Pancreatic Beta-Cell
Philippaert, K., & Vennekens, R. (2017) · CRC Press eBooks · doi:10.4324/9781315152837-12 · Cited by 13
Energetics of Glucose Metabolism: A Phenomenological Approach to Metabolic Network Modeling
Diederichs, F. (2010) · International Journal of Molecular Sciences · doi:10.3390/ijms11082921 · Cited by 3
Upregulation of α-ENaC induces pancreatic β-cell dysfunction, ER stress, and SIRT2 degradation
Zhang, X., Zhang, D., Huo, L., Zhou, X., Zhang, J., Li, M., Su, D., Sun, P., Chen, F., & Liang, X. (2023) · Journal of Biomedical Research · doi:10.7555/jbr.37.20230128 · Cited by 2
Environmentally occurring aflatoxins B1 and M1 notifyably harms pancreatic islets
Mehrzad, J., Salehi, T. Z., Khosravi, A., Hosseinkhani, S., Tahamtani, Y., Hajizadeh-Saffar, E., Moazenchi, M., & Malvandi, A. (2021) · Toxin Reviews · doi:10.1080/15569543.2021.2010758 · Cited by 2
“Glucose activates pancreatic cells (Drews et al. 2010a, 2010b, Malvandi et al. 2019), and activated islets showed more susceptibility to AFB1 and AFM1 toxicity.”
BackgroundInfluentialDüfer, M. (2018) · Journal of Physiology · doi:10.1113/jp275329 · Cited by 2
“Electrical excitability is a key feature of all three cell types (Drews et al. 2010).”
BackgroundSelf-citationThe Ca2+-Activated Monovalent Cation-Selective Channels TRPM4 and TRPM5
Colsoul, B., Kecskés, M., Philippaert, K., Menigoz, A., & Vennekens, R. (2012) · Methods in pharmacology and toxicology · doi:10.1007/978-1-62703-077-9_6 · Cited by 2
Determination of Beta-Cell Function: Ion Channel Function in Beta Cells
Düfer, M. (2012) · Humana Press eBooks · doi:10.1007/978-1-62703-068-7_13 · Cited by 3
Self-citationTracing Patterns in Electrophysiological Time Series Data
Hüwel, J. D., Gresch, A., Berns, F., Koch, R., Düfer, M., & Beecks, C. (2022) · International Conference on Data Science and Advanced Analytics · doi:10.1109/dsaa54385.2022.10032339 · Cited by 1
“The rising membrane potential opens voltage-gated calcium channels and more calcium ions flow into the cell, triggering insulin secretion [20].”
BackgroundSelf-citationPohorec, V., Bombek, L. K., Klemen, M., Dolenšek, J., & Stožer, A. (2022) · bioRxiv · doi:10.1101/2022.01.14.476318 · Cited by 1
The role of Npas4 and Rgs2 in the regulation of pancreatic β-cell function
Speckmann, T. (2019) · doi:10.14288/1.0380061 · Cited by 1
“Because the resting β-cell membrane potential is hyperpolarized relative to the extracellular milieu (-80 mV to -60 mV), the intracellular buildup of positively charged potassium ions [84] causes membrane depolarization, and at a membrane potential above -50 mV (-60 mV in human β-cells), action potentials are elicited…”
BackgroundRedox Signaling is Essential for Insulin Secretion
Ježek, P., Holendová, B., Jabůrek, M., Tauber, J. A., Dlasková, A., & Plecitá‐Hlavatá, L. (2021) · IntechOpen eBooks · doi:10.5772/intechopen.94312
The Problem of Outward Cellular Electric Current
Noble, M. (2019) · Online Journal of Cardiovascular Research · doi:10.33552/ojcr.2019.01.000521
“Where do the electrons come from when there is a hyperpolarisation burst? The same authors [3] reviewed all the ion channels in islet cells and concluded that the depolarizing current of beta-cells occurred by an as yet unknown ion channel.”
BackgroundGómez‐Barriocanal, J. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/249805 · Cited by 1
The Role of Membrane Excitability in Insulin Regulation
Emfinger, C. H. (2018) · doi:10.7936/7w5n-cr33
“The transient-receptor potential channels (TRP channels) are important non-selective cation channels that contribute to incretin-induced depolarization and contribute to calcium oscillations (Drews et al., 2010).”
BackgroundInfluential
Metadata
- Authors
- Drews, G., Krippeit-Drews, P., & Düfer, M.
- Affiliations
- University of Tübingen (DE)
- Corresponding author
- Drews, Gisela
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer Netherlands
- Published
- 2010
- Volume
- 654
- Pages
- 115-163
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W1886288445
- Cited by
- 152
- References
- 0
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 9 · 2022: 8 · 2021: 14 · 2020: 7 · 2019: 4 · 2018: 10 · 2017: 11 · 2016: 4 · 2015: 10 · 2014: 15 · 2013: 16 · 2012: 16
- FWCI
- 135.74
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- pancreatic beta cells, stimulus-secretion coupling, ATP-sensitive potassium channels, beta-cell electrical activity, glucose-stimulated insulin secretion, L-type calcium channels, oxidative stress, alpha cells, delta cells, ion channels, membrane potential, exocytosis, voltage-gated sodium channels
- MeSH terms
- Adenosine Triphosphate, Animals, Calcium, Cell Membrane, Electrophysiology, Glucose, Humans, Ion Channels, Islets of Langerhans, Membrane Potentials, Oscillometry, Potassium Channels, Mice, Knockout, Oxidative Stress, Mice
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