ArticleEuropean biophysics journal : EBJ1994
Inactivation of voltage-dependent calcium current in an insulinoma cell line.
Article in European biophysics journal : EBJ, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Beta-Cell Ion Channels and Their Role in Regulating Insulin Secretion.Comprehensive Physiology · 2021Review
- Regulation of insulin secretion in islets of Langerhans by Ca(2+)channels.The Journal of membrane biology · 2004Review
- Voltage-operated calcium channel heterogeneity in pancreatic beta cells: physiopathological implications.Journal of bioenergetics and biomembranes · 2003Review
- Modulation and pharmacology of low voltage-activated ("T-Type") calcium channels.Journal of bioenergetics and biomembranes · 2003Review
- Localized calcium influx in pancreatic beta-cells: its significance for Ca2+-dependent insulin secretion from the islets of Langerhans.Endocrine · 2000Review
- A single non-L-, non-N-type Ca2+ channel in rat insulin-secreting RINm5F cells.Pflugers Archiv : European journal of physiology · 1996Article
- Block of non-L-, non-N-type Ca2+ channels in rat insulinoma RINm5F cells by omega-agatoxin IVA and omega-conotoxin MVIIC.Pflugers Archiv : European journal of physiology · 1995Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have studied the mechanism of Ca current inactivation in the beta-cell line HIT-T15 by conventional and perforated patch recording techniques, using two pulse voltage protocols and a combination of current and tail current measurements. In 5 mM Ca, from a holding potential of -80 mV, the maximum current showed a complex time course of inactivation: a relatively fast, double exponential inactivation (tau h1 approximately 12 ms and tau h2 approximately 60 ms) and a very slowly inactivating component (tau > 1 s). The faster component (tau h1) was due to the voltage-dependent inactivation of a low-threshold-activated (LVA), T-type current, which deactivates more slowly (tau approximately 3-5 ms) than the other components (tau approximately 0.2-0.3 ms). The intermediate component (tau h2) was due to the Ca-dependent inactivation of a portion of the high-threshold-activated (HVA) current. A saturating dose of the dihydropyridine (DHP) nifedipine (10 microM) did not affect the LVA current, but inhibited by 68 +/- 5% the transient, Ca-sensitive portion of the HVA current and by 33 +/- 12% the long lasting component. We suggest that three components of the calcium current can be resolved in HIT cells and the main target of DHPs is a HVA current, which inactivates faster than the DHP-resistant HVA component and does so primarily through calcium influx.
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