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Cited by 135Ion channel regulation and functionCardiac electrophysiology and arrhythmiasNeuroblastoma Research and Treatments

Potassium current suppression by quinidine reveals additional calcium currents in neuroblastoma cells.

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Fishman, M C, Spector, I·1981·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.78.8.5245PMC PMC320388
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Abstract

Quinine and quinidine have been evaluated with regard to their effects on the electrical activity of neuroblastoma cells. Under voltage-clamp conditions, we have found that quinine and quinidine block both the voltage-dependent and Ca2+-dependent K+ conductances. Blockage of the voltage-dependent K+ channel is manifest as an increase in the amplitude and in the duration of the action potential. Blockage of the Ca2+-dependent K+ channel in Na+-free (replaced by Tris) solutions containing 6.8 mM Ca2+ and tetraethylammonium ion or 4-aminopyridine (to block the voltage-dependent K+ current) is seen as a further prolongation of the Ca2+ action potential and diminution of the after-hyperpolarization. A critical role of the Ca2+-dependent K+ conductance in modulation of the rate and duration of trains of Ca2+ action potentials is shown by the use of low concentrations (5-40 microM) of quinine or quinidine, which diminish the Ca2+-dependent K+ conductance in a graded manner. After complete blockade of K+ currents, the peak Ca2+ currents are enhanced at all voltages, especially at values more positive than -30 mV, where a steady-state inward current appears as well. In this same voltage range, the decay of the Ca2+ current exhibits two time constants--that of the transient inward current, which is about 20 msec, and a much slower (approximately 2000 msec) component. It is suggested that neuroblastoma cells have two types of calcium channels--one which generates the Ca2+ action potential and a second, distinguished by activation at more depolarized levels and by a slow rate of inactivation, which underlies the calcium entry necessary to activate the Ca2+-dependent K+ conductance.

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  • Quinine (0.5-1 mM) abolished single channel and whole-cell currents in both cell types.

    “In addition, quinine, another K⁺ channel blocker (6), abolished single channel and whole-cell currents in both types of cells (at 0.5–1 mm; data not shown).”

    From Potassium Channels in Motor Cells of <i>Samanea saman</i> (1988) · cites this paper as [6]

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Research works printed but not linked: 27

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Cited by

Sorted by citations

Authors
Fishman, M. C., & Spector, I.
Affiliations
National Institutes of Health (US)
ORCID
Fishman, M C
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
1981-08
Volume
78
Issue
8
Pages
5245-5249
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.78.8.5245
PMC
PMC320388
OpenAlex
W2022573440
Cited by
135
References
0
Citations by year
2023: 2 · 2018: 2 · 2016: 1 · 2015: 2 · 2014: 1 · 2013: 2 · 2012: 2
FWCI
2.47
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Health Sciences › Medicine › Neurology › Neuroblastoma Research and Treatments
Keywords
quinidine, quinine, calcium-activated potassium current, voltage-dependent potassium current, calcium action potentials, calcium channels, neuroblastoma cells, afterhyperpolarization, calcium channel inactivation, calcium inward current
MeSH terms
Action Potentials, Animals, Calcium, Cell Line, Ion Channels, Neuroblastoma, Potassium, Quinidine, Quinine, Mice

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