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This Article Full Text Full Text (PDF) All Versions of this Article: 556/1/121    most recent jphysiol.2003.056168v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Blumenstein, Y. Articles by Dascal, N. Search for Related Content PubMed PubMed Citation Articles by Blumenstein, Y. Articles by Dascal, N.

¹ Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel² Department of Cellular Membranology, Bogomoletz Institute of Physiology, Kyiv 01024, Ukraine

N-type voltage-dependent Ca²⁺ channels (N-VDCCs) play important roles in neurotransmitter release and certain postsynaptic phenomena. These channels are modulated by a number of intracellular factors, notably by Gß subunits of G proteins, which inhibit N-VDCCs in a voltage-dependent (VD) manner. Here we show that an increase in intracellular Na⁺ concentration inhibits N-VDCCs in hippocampal pyramidal neurones and in Xenopus oocytes. In acutely dissociated hippocampal neurones, Ba²⁺ current via N-VDCCs was inhibited by Na⁺ influx caused by the activation of NMDA receptor channels. In Xenopus oocytes expressing N-VDCCs, Ba²⁺ currents were inhibited by Na⁺ influx and enhanced by depletion of Na⁺, after incubation in a Na⁺-free extracellular solution. The Na⁺-induced inhibition was accompanied by the development of VD facilitation, a hallmark of a Gß-dependent process. Na⁺-induced regulation of N-VDCCs is Gß dependent, as suggested by the blocking of Na⁺ effects by Gß scavengers and by excess Gß, and may be mediated by the Na⁺-induced dissociation of Gß heterotrimers. N-VDCCs may be novel effectors of Na⁺ion, regulated by the Na⁺ concentration via Gß.

(Received 30 September 2003; accepted after revision 15 January 2004; first published online 23 January 2004)
Corresponding author N. Dascal: Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv 69978, Israel. Email: dascaln{at}post.tau.ac.il

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