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Molecular Pharmacology

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Research ArticleArticle

Plasma Membrane Depolarization and Disturbed Na+Homeostasis Induced by the Protonophore Carbonyl Cyanide-p-trifluoromethoxyphenyl-hydrazon in Isolated Nerve Terminals

Laszlo Tretter, Christos Chinopoulos and Vera Adam-Vizi
Molecular Pharmacology April 1998, 53 (4) 734-741; DOI: https://doi.org/10.1124/mol.53.4.734
Laszlo Tretter
Department of Medical Biochemistry, Neurochemical Group, Semmelweis University of Medicine, Budapest, Hungary
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Christos Chinopoulos
Department of Medical Biochemistry, Neurochemical Group, Semmelweis University of Medicine, Budapest, Hungary
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Vera Adam-Vizi
Department of Medical Biochemistry, Neurochemical Group, Semmelweis University of Medicine, Budapest, Hungary
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Abstract

The effect of the protonophore carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazon (FCCP) was studied on the intracellular [Na+], pH, and plasma membrane potential in isolated nerve terminals. FCCP induced a rise of [Na+]i at, and even below, the concentrations (0.025–1 μm) in which it is usually used in intact cells to eliminate Ca2+ uptake by mitochondria. The FCCP-induced increase of [Na+]i correlates with a fall in both the ATP level and the ATP/ADP ratio. In addition, a sudden rise of the intracellular proton concentration ([H+]i) from 83 ± 0.4 to 124 ± 0.7 nm was observed on the addition of FCCP (1 μm). Parallel with the rise in [H+]i, an abrupt depolarization was detected, followed by a slower decrease in the plasma membrane potential. Both the extent of the pHi change and the fast depolarization of the plasma membrane were proportional to the proton electrochemical gradient across the plasma membrane; when this gradient was increased, greater depolarization was detected. The slower decrease of the membrane potential after the fast initial depolarization was abolished when the medium contained no Na+. It is concluded that FCCP (1) gives rise to a depolarization by setting the plasma membrane potential close to the proton equilibrium potential and (2) enhances the intracellular [Na+] as a consequence of an insufficient ATP level and ATP/ADP ratio to fuel the Na+,K+/ATPase. Because both disturbed Na+ homeostasis and plasma membrane depolarization could profoundly interfere with Ca2+ homeostasis in the presence of protonophores, consideration given to these alterations may help to clarify the cellular Ca2+ sequestration processes.

Footnotes

    • Received October 10, 1997.
    • Accepted December 16, 1997.
  • Send reprint requests to: Vera Adam-Vizi, M.D., Ph.D., Department of Medical Biochemistry, Semmelweis University of Medicine, P. O. Box 262, Budapest, H-1444, Hungary. E-mail:av{at}puskin.sote.hu

  • The work was supported by grants from the Hungarian Scientific Research Fund, the Hungarian Ministry of Welfare, and the Hungarian Academy of Sciences (V.A.-V).

  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 53 (4)
Molecular Pharmacology
Vol. 53, Issue 4
1 Apr 1998
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Research ArticleArticle

Plasma Membrane Depolarization and Disturbed Na+Homeostasis Induced by the Protonophore Carbonyl Cyanide-p-trifluoromethoxyphenyl-hydrazon in Isolated Nerve Terminals

Laszlo Tretter, Christos Chinopoulos and Vera Adam-Vizi
Molecular Pharmacology April 1, 1998, 53 (4) 734-741; DOI: https://doi.org/10.1124/mol.53.4.734

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Research ArticleArticle

Plasma Membrane Depolarization and Disturbed Na+Homeostasis Induced by the Protonophore Carbonyl Cyanide-p-trifluoromethoxyphenyl-hydrazon in Isolated Nerve Terminals

Laszlo Tretter, Christos Chinopoulos and Vera Adam-Vizi
Molecular Pharmacology April 1, 1998, 53 (4) 734-741; DOI: https://doi.org/10.1124/mol.53.4.734
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