Na+ current properties in islet α‐ and β‐cells reflect cell‐specific Scn3a and Scn9a expression
Open accessAbstract
Key points: α‐ and β‐cells express both Na v 1.3 and Na v 1.7 Na+ channels but in different relative amounts. The differential expression explains the different properties of Na+ currents in α‐ and β‐cells. Na v 1.3 is the functionally important Na+ channel α subunit in both α‐ and β‐cells. Islet Na v 1.7 channels are locked in an inactive state due to an islet cell‐specific factor. Mouse pancreatic β‐ and α‐cells are equipped with voltage‐gated Na+ currents that inactivate over widely different membrane potentials (half‐maximal inactivation (V0.5) at −100 mV and −50 mV in β‐ and α‐cells, respectively). Single‐cell PCR analyses show that both α‐ and β‐cells have Na v 1.3 (Scn3) and Na v 1.7 (Scn9a) α subunits, but their relative proportions differ: β‐cells principally express Na v 1.7 and α‐cells Na v 1.3. In α‐cells, genetically ablating Scn3a reduces the Na+ current by 80%. In β‐cells, knockout of Scn9a lowers the Na+ current by >85%, unveiling a small Scn3a‐dependent component. Glucagon and insulin secretion are inhibited in Scn3a−/− islets but unaffected in Scn9a‐deficient islets. Thus, Na v 1.3 is the functionally important Na+ channel α subunit in both α‐ and β‐cells because Na v 1.7 is largely inactive at physiological membrane potentials due to its unusually negative voltage dependence of inactivation. Interestingly, the Na v 1.7 sequence in brain and islets is identical and yet the V0.5 for inactivation is >30 mV more negative in β‐cells. This may indicate the presence of an intracellular factor that modulates the voltage dependence of inactivation.
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In most mouse β-cells, TTX-sensitive Na+ channels are not involved in action potential firing.
“For example, activation of TTX-sensitive Na+ channels plays a prominent role in human β-cell action potential firing at low glucose but not at high glucose (90, 521) - and in most mouse β-cells it is not involved in action potential firing at all (761).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
The Results section ('Role of Na+ channels in islet cell electrical activity: effects of TTX'; page unavailable) reports that TTX markedly reduced action-potential amplitude in three of six mouse β-cells at 8 mM glucose and significantly reduced peak voltage at 20 mM glucose. Although it barely affected the other three cells tested at 8 mM, the Discussion ('Role of Na+ channels in β-cells'; page unavailable) concludes that a TTX-sensitive Na+ current likely contributes to action-potential firing. The source therefore does not support saying these channels are uninvolved in most mouse β-cells at all. (LLM, conf=0.89)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredAt glucose concentrations just above the threshold for electrical activity (~6 mM), only 7% of β-cells exhibit [Ca2+]i oscillations, but as glucose increases the fraction of active β-cells increases.
“At gl(441)ucose concentrations just above the threshold for electrical activity (~6 mM), only 7% of the β-cells exhibit [Ca2+]i oscillations (761), but as the glucose concentration is increased, the fraction of active β-cells increases.”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
The Results section (Fig. 5A; page unavailable in our copy) reports [Ca2+]i oscillations at 6 mM glucose in 6 of 110 cells, or about 5.5%, not 7%. It also reports that raising glucose to 20 mM recruited additional β-cells, supporting the claimed increase in the active fraction. The paper notes that some cells responding at 6 mM may have been δ-cells, although it confirmed that some β-cells responded. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe mouse β-cell Na+ current appears particularly important at low glucose concentrations, because the increase in electrical activity, [Ca2+]i and insulin secretion evoked by 6 mM glucose are all strongly reduced by TTX.
“The mouse β-cell Na+ current appears to be particularly important at low glucose concentrations, because the increase in electrical activity, [Ca2+]i and insulin secretion evoked by 6 mM glucose are all strongly reduced by TTX (761).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
The Results section reports that TTX strongly reduced 6 mM glucose–evoked calcium oscillations in the small subset of responding cells and inhibited insulin secretion by 74 ± 8% at 6 mM glucose. But the paper tested TTX’s effect on β-cell electrical activity at 8 and 20 mM glucose, not 6 mM, and found variable effects at 8 mM. Thus, the claim’s electrical-activity component at 6 mM is not established by this source. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn ~30% of β-cells an additional Na+ current component is present, accounting for 15-25% of the total Na+ current (~150 pA), with inactivation half-complete at -40 mV, persisting at physiological membrane potentials and capable of contributing to the upstroke of the action potential.
“Not all β-cells conform to this picture, however: in ~30% of β-cells an additional Na+ current component is present, which accounts for 15-25% of the total Na+ current (i.e. ~150 pA) (709, 761). As its inactivation is half-complete at -40 mV, this Na+ current component persists at physiological membrane potentials and is therefore capable of contributing to the upstroke of the action potential (76”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe mouse β-cell Na+ channel is highly unusual in the voltage dependence of its inactivation; in most β-cells it inactivates at such negative membrane potentials that little or no Na+ current remains within the physiological range.
“The mouse (and rat) β-cell Na+ channel is highly unusual in the voltage dependence of its inactivation. In most β-cells, it inactivates at such negative membrane potentials that little or no Na+ current remains within the physiological range of membrane potentials (221, 514, 761) (Figure 10).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
In 30% of β-cells, voltage-gated Na+ channels also contribute to action potential firing.
“In 30% of β-cells, voltage-gated Na+ channels also contribute to action potential firing (761).”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
Increasing glucose recruits quiescent β-cells and causes a concentration-dependent increase in electrical activity of individual β-cells.
“Although increasing glucose ‘recruits’ quiescent β-cells (402, 761), there is also a concentration-dependent increase in the electrical activity of individual β-cells.”
From Pancreatic β-Cell Electrical Activity and Insulin Secretion: Of Mice and Men (2018) · cites this paper as [761]
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Glucagon: From Gene Regulation to Secretion
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- Authors
- Zhang, Q., Chibalina, M. V., Bengtsson, M., Groschner, L. N., Ramracheya, R., Rorsman, N. J. G., Leiss, V., Nassar, M. A., Welling, A., Gribble, F. M., Reimann, F., Hofmann, F., Wood, J. N., Ashcroft, F. M., & Rorsman, P.
- Affiliations
- Churchill Hospital (GB)
- Technical University of Munich (DE)
- University College London (GB)
- University of Cambridge (GB)
- University of Oxford (GB)
- Corresponding author
- Rorsman, Patrik
- ORCID
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2014-10-31
- Volume
- 592
- Issue
- 21
- Pages
- 4677-4696
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC4253470
- OpenAlex
- W1608643486
- Cited by
- 90
- References
- 50
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 9 · 2023: 7 · 2022: 8 · 2021: 14 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 8
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Physiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Funders
- Wellcome Trust (884655, 089795, 095531)
- European Union (322620)
- 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
- voltage-gated sodium channels, Nav1.3, Nav1.7, SCN3A, SCN9A, pancreatic beta cells, sodium current, voltage-dependent inactivation, insulin secretion, glucagon secretion, knockout mice
- MeSH terms
- Insulin Secretion, Animals, Gene Expression Regulation, Glucose, Humans, Insulin, Mice, Inbred C57BL, Neurotoxins, Sodium, Mice, Knockout, Protein Isoforms, Protein Subunits, Glucagon-Secreting Cells, Insulin-Secreting Cells, Mice, HEK293 Cells, NAV1.3 Voltage-Gated Sodium Channel, NAV1.7 Voltage-Gated Sodium Channel
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