Veratridine blocks voltage-gated potassium current in human T lymphocytes and in mouse neuroblastoma cells

(i) Effects of veratridine on ionic conductances of human peripheral blood T lymphocytes have been investigated using the whole-cell patch-clamp technique. (ii) Veratridine reduces the net outward current evoked by membrane depolarizations. The reduction originates from block of a 4-aminopyridine-se...

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Veröffentlicht in:The Journal of membrane biology 1994-02, Vol.137 (3), p.205-214
Hauptverfasser: BERHEUGEN, J. A. H, OORTGIESEN, M, VIJVERBERG, H. P. M
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container_issue 3
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container_title The Journal of membrane biology
container_volume 137
creator BERHEUGEN, J. A. H
OORTGIESEN, M
VIJVERBERG, H. P. M
description (i) Effects of veratridine on ionic conductances of human peripheral blood T lymphocytes have been investigated using the whole-cell patch-clamp technique. (ii) Veratridine reduces the net outward current evoked by membrane depolarizations. The reduction originates from block of a 4-aminopyridine-sensitive, voltage-gated K+ current. (iii) Human T lymphocytes do not appear to express voltage-gated Na+ channels, since inward currents are observed neither in control nor in veratridine- and bretylium-exposed lymphocytes. (iv) The effect of veratridine consists of an increase in the rate of decay of the voltage-gated K+ current and a reduction of the peak current amplitude. Both effects depend on veratridine concentration. Half-maximum block occurs at 97 microM and the time constant of decay is reduced by 50% at 54 microM of veratridine. (v) Possible mechanisms of veratridine action are discussed. The increased rate of K+ current decay is most likely due to open channel block. The decrease of current amplitude may involve an additional mechanism. (vi) In cultured mouse neuroblastoma N1E-115 cells, veratridine blocks a component of voltage-gated K+ current, in addition to its effect on voltage-gated Na+ current. This result shows that the novel effect of veratridine is not confined to lymphocytes.
doi_str_mv 10.1007/BF00232589
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(v) Possible mechanisms of veratridine action are discussed. The increased rate of K+ current decay is most likely due to open channel block. The decrease of current amplitude may involve an additional mechanism. (vi) In cultured mouse neuroblastoma N1E-115 cells, veratridine blocks a component of voltage-gated K+ current, in addition to its effect on voltage-gated Na+ current. This result shows that the novel effect of veratridine is not confined to lymphocytes.</description><identifier>ISSN: 0022-2631</identifier><identifier>EISSN: 1432-1424</identifier><identifier>DOI: 10.1007/BF00232589</identifier><identifier>PMID: 8182730</identifier><identifier>CODEN: JMBBBO</identifier><language>eng</language><publisher>New York, NY: Springer</publisher><subject>4-Aminopyridine - pharmacology ; Animals ; Biological and medical sciences ; Cadmium - pharmacology ; Cell membranes. Ionic channels. 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(iv) The effect of veratridine consists of an increase in the rate of decay of the voltage-gated K+ current and a reduction of the peak current amplitude. Both effects depend on veratridine concentration. Half-maximum block occurs at 97 microM and the time constant of decay is reduced by 50% at 54 microM of veratridine. (v) Possible mechanisms of veratridine action are discussed. The increased rate of K+ current decay is most likely due to open channel block. The decrease of current amplitude may involve an additional mechanism. (vi) In cultured mouse neuroblastoma N1E-115 cells, veratridine blocks a component of voltage-gated K+ current, in addition to its effect on voltage-gated Na+ current. This result shows that the novel effect of veratridine is not confined to lymphocytes.</description><subject>4-Aminopyridine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cadmium - pharmacology</subject><subject>Cell membranes. 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H</creatorcontrib><creatorcontrib>OORTGIESEN, M</creatorcontrib><creatorcontrib>VIJVERBERG, H. P. M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>The Journal of membrane biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BERHEUGEN, J. A. H</au><au>OORTGIESEN, M</au><au>VIJVERBERG, H. P. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Veratridine blocks voltage-gated potassium current in human T lymphocytes and in mouse neuroblastoma cells</atitle><jtitle>The Journal of membrane biology</jtitle><addtitle>J Membr Biol</addtitle><date>1994-02-01</date><risdate>1994</risdate><volume>137</volume><issue>3</issue><spage>205</spage><epage>214</epage><pages>205-214</pages><issn>0022-2631</issn><eissn>1432-1424</eissn><coden>JMBBBO</coden><abstract>(i) Effects of veratridine on ionic conductances of human peripheral blood T lymphocytes have been investigated using the whole-cell patch-clamp technique. (ii) Veratridine reduces the net outward current evoked by membrane depolarizations. The reduction originates from block of a 4-aminopyridine-sensitive, voltage-gated K+ current. (iii) Human T lymphocytes do not appear to express voltage-gated Na+ channels, since inward currents are observed neither in control nor in veratridine- and bretylium-exposed lymphocytes. (iv) The effect of veratridine consists of an increase in the rate of decay of the voltage-gated K+ current and a reduction of the peak current amplitude. Both effects depend on veratridine concentration. Half-maximum block occurs at 97 microM and the time constant of decay is reduced by 50% at 54 microM of veratridine. (v) Possible mechanisms of veratridine action are discussed. The increased rate of K+ current decay is most likely due to open channel block. The decrease of current amplitude may involve an additional mechanism. (vi) In cultured mouse neuroblastoma N1E-115 cells, veratridine blocks a component of voltage-gated K+ current, in addition to its effect on voltage-gated Na+ current. 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subjects 4-Aminopyridine - pharmacology
Animals
Biological and medical sciences
Cadmium - pharmacology
Cell membranes. Ionic channels. Membrane pores
Cell structures and functions
Dose-Response Relationship, Drug
Drug Interactions
Electrophysiology
Fundamental and applied biological sciences. Psychology
Humans
In Vitro Techniques
Membrane Potentials
Mice
Molecular and cellular biology
Neuroblastoma - metabolism
Potassium - metabolism
Potassium Channels - drug effects
Potassium Channels - metabolism
T-Lymphocytes - drug effects
T-Lymphocytes - metabolism
Tumor Cells, Cultured - drug effects
Tumor Cells, Cultured - metabolism
Veratridine - administration & dosage
Veratridine - pharmacology
title Veratridine blocks voltage-gated potassium current in human T lymphocytes and in mouse neuroblastoma cells
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