Naunyn-Schmiedeberg's Archives of Pharmacology

, Volume 362, Issue 4, pp 440–443

Acamprosate inhibits Ca2+ influx mediated by NMDA receptors and voltage-sensitive Ca2+ channels in cultured rat mesencephalic neurones

  • Clemens Allgaier
  • Heike Franke
  • Helga Sobottka
  • Peter Scheibler
Short Communication

DOI: 10.1007/s002100000285

Cite this article as:
Allgaier, C., Franke, H., Sobottka, H. et al. Naunyn-Schmied Arch Pharmacol (2000) 362: 440. doi:10.1007/s002100000285

Abstract

Acamprosate has recently been introduced in relapse prophylaxis in weaned alcoholics. Using fura-2 microfluorimetry, the present study investigates whether acamprosate affects N-methyl-d-aspartate (NMDA) or K+-induced changes in free intracellular Ca2+ concentration ([Ca2+]i) in rat cultured mesencephalic neurones. Both application of NMDA (plus glycine) and elevation of extracellular K+ induced rapid increases in [Ca2+]i which respectively were insensitive and sensitive to ω-conotoxin (ω-CTX) MVIIC, a blocker of voltage-dependent Ca2+ channels (VDCCs). Acamprosate (100 µM and 300 µM) significantly attenuated the response induced by NMDA as well as that induced by K+ in a concentration-dependent manner. Concurrent application of ω-CTX MVIIC and acamprosate impaired the K+-induced increase in [Ca2+]i to the same extent as ω-CTX MVIIC alone. The present data suggest that acamprosate inhibits Ca2+ influx through both NMDA receptors and VDCCs.

Acamprosate NMDA receptor Voltage-dependent Ca2+ channels ω-Conotoxin MVIIC Fura-2 Intracellular Ca2+ concentration Cultured mesencephalic neurones 

Copyright information

© Springer-Verlag 2000

Authors and Affiliations

  • Clemens Allgaier
    • 1
  • Heike Franke
    • 1
  • Helga Sobottka
    • 1
  • Peter Scheibler
    • 1
  1. 1.Rudolf-Boehm-Institut für Pharmakologie und Toxikologie, Universität Leipzig, Härtelstrasse 16/18, D-04107 LeipzigGermany

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