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Research ArticleArticle

Calcium Channels Involved in K+- and Veratridine-Induced Increase of Cytosolic Calcium Concentration in Human Cerebral Cortical Synaptosomes

Wolfgang Meder, Klaus Fink, Josef Zentner and Manfred Göthert
Journal of Pharmacology and Experimental Therapeutics September 1999, 290 (3) 1126-1131;
Wolfgang Meder
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Klaus Fink
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Josef Zentner
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Manfred Göthert
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Abstract

Human cerebral cortical synaptosomes were used to study voltage-dependent Ca2+ channels mediating calcium influx in human axon terminals. Synaptosomes were depolarized by elevation of the extracellular K+ concentration by 30 mM or by the addition of veratridine (10 μM). Increase in cytosolic concentration of calcium [Ca2+]i induced by either stimulus was abolished in the absence of extracellular Ca2+ions. ω-Agatoxin IVA inhibited the K+-induced [Ca2+]i increase concentration-dependently (IC50: 113 nM). ω-Conotoxin GVIA (0.1 μM) inhibited K+-induced [Ca2+]iincrease by 20%. ω-Conotoxin MVIIC (0.2 μM) caused an inhibition by 85%. Nifedipine (1 μM) had no effect on K+-induced [Ca2+]i increase. Veratridine-induced increase in [Ca2+]i was inhibited by ω-conotoxin GVIA (0.1 μM) and ω-Agatoxin IVA (0.2 μM; by about 25 and 45%, respectively). Nifedipine inhibited the veratridine-evoked [Ca2+]i increase concentration-dependently (IC50: 4.9 nM); Bay K 8644 (3 μM) shifted the nifedipine concentration-response curve to the right. Mibefradil (10 μM) abolished the increase in [Ca2+]i evoked by K+ and reduced the increase evoked by veratridine by almost 90%. KB-R7943 (3 μM) an inhibitor of the Na+/Ca2+ exchanger NCX1, decreased the increase in [Ca2+]i evoked by veratridine by approximately 20%. It is concluded that the increase in [Ca2+]i after K+ depolarization caused by Ca2+ influx predominantly via P/Q-type Ca2+ channels and after veratridine depolarization via N- and P/Q-type, but also by L-type Ca2+ channels. The toxin- and nifedipine-resistant fraction of the veratridine response may result both from influx via R-type Ca2+ channels and by Ca2+ inward transport via Na+/Ca2+exchanger.

Footnotes

  • Send reprint requests to: Dr. Manfred Göthert, Dept. of Pharmacology and Toxicology, University of Bonn, Reuterstraße 2b, 53113 Bonn, Germany. E-mail: finkk{at}uni-bonn.de

  • ↵1 This study was supported by the Deutsche Forschungsgemeinschaft (SFB 400), the Graduiertenkolleg “Pathogenese von Krankheiten des Nervensystems” (Deutsche Forschungsgemeinschaft), and the European Community (Biotechnology Program).

  • Abbreviations:
    VDCC
    voltage-dependent calcium channel
    fura-2/AM
    fura-2 acetoxymethyl ester
    [Ca2+]i
    cytosolic concentration of calcium
    TTX
    tetrodotoxin
    PSS
    physiological salt solution
    ω-CTx GVIA
    ω-conotoxin GVIA
    ω-AgaTx IVA
    ω-agatoxin IVA
    ω-CTx MVIIC
    ω-conotoxin MVIIC
    • Received November 10, 1998.
    • Accepted May 24, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 290 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 290, Issue 3
1 Sep 1999
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Research ArticleArticle

Calcium Channels Involved in K+- and Veratridine-Induced Increase of Cytosolic Calcium Concentration in Human Cerebral Cortical Synaptosomes

Wolfgang Meder, Klaus Fink, Josef Zentner and Manfred Göthert
Journal of Pharmacology and Experimental Therapeutics September 1, 1999, 290 (3) 1126-1131;

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Research ArticleArticle

Calcium Channels Involved in K+- and Veratridine-Induced Increase of Cytosolic Calcium Concentration in Human Cerebral Cortical Synaptosomes

Wolfgang Meder, Klaus Fink, Josef Zentner and Manfred Göthert
Journal of Pharmacology and Experimental Therapeutics September 1, 1999, 290 (3) 1126-1131;
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