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

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.

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Authors and Affiliations

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

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1. Clemens Allgaier
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2. Heike Franke
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3. Helga Sobottka
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4. Peter Scheibler
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Allgaier, C., Franke, H., Sobottka, H. et al. Acamprosate inhibits Ca2+ influx mediated by NMDA receptors and voltage-sensitive Ca2+ channels in cultured rat mesencephalic neurones.Naunyn-Schmied Arch Pharmacol 362, 440–443 (2000). https://doi.org/10.1007/s002100000285

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• Received: 05 April 2000
• Accepted: 22 May 2000
• Published: 17 August 2000
• Issue Date: November 2000
• DOI: https://doi.org/10.1007/s002100000285