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Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, D-40225 Düsseldorf, Germany

Address correspondence to Dorothee Günzel at her present address: Charité - Universitätsmedizin Berlin, Campus Benjamin Franklin, Institut für klinische Physiologie, Hindenburgdamm 30, 12200 Berlin, Germany. Fax: (49) 30-8445 4239; email: dorothee.guenzel{at}medizin.fu-berlin.de

In Retzius neurones of the medicinal leech, Hirudo medicinalis, kainate activates ionotropic glutamate receptors classified as AMPA/kainate receptors. Activation of the AMPA/kainate receptor–coupled cation channels evokes a marked depolarization, intracellular acidification, and increases in the intracellular concentrations of Na⁺ ([Na⁺]_i) and Ca²⁺. Qualitatively similar changes are observed upon the application of carbachol, an activator of acetylcholine receptor-coupled cation channels. Using multibarrelled ion-selective microelectrodes it was demonstrated that kainate, but not carbachol, caused additional increases in the intracellular free Mg²⁺ concentration ([Mg²⁺]_i). Experiments were designed to investigate whether this kainate-induced [Mg²⁺]_i increase was due to a direct Mg²⁺ influx through the AMPA/kainate receptor–coupled cation channels or a secondary effect due to the depolarization or the ionic changes. It was found that: (a) Similar [Mg²⁺]_i increases were evoked by the application of glutamate or aspartate. (b) All kainate-induced effects were inhibited by the glutamatergic antagonist DNQX. (c) The magnitude of the [Mg²⁺]_i increases depended on the extracellular Mg²⁺ concentration. (d) A reduction of the extracellular Ca²⁺ concentration increased kainate-induced [Mg²⁺]_i increases, excluding possible Ca²⁺ interference at the Mg²⁺-selective microelectrode or at intracellular buffer sites. (e) Neither depolarizations evoked by the application of 30 mM K⁺, nor [Na⁺]_i increases induced by the inhibition of the Na⁺/K⁺ ATPase caused comparable [Mg²⁺]_i increases. (f) Inhibitors of voltage-dependent Ca²⁺ channels did not affect the kainate-induced [Mg²⁺]_i increases. Moreover, previous experiments had already shown that intracellular acidification evoked by the application of 20 mM propionate did not cause changes in [Mg²⁺]_i. The results indicate that kainate-induced [Mg²⁺]_i increases in leech Retzius neurones are due to an influx of extracellular Mg²⁺ through the AMPA/kainate receptor–coupled cation channel. Mg²⁺ may thus act as an intracellular signal to distinguish between glutamatergic and cholinergic activation of leech Retzius neurones.

Key Words: magnesium • ion-selective microelectrode • glutamate receptor • ion channels • divalent cations

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This article has been cited by other articles:

				D. Gunzel, K. Hintz, S. Durry, and W.-R. Schlue Mg2+-Malate Co-Transport, a Mechanism for Na+-Independent Mg2+ Transport in Neurons of the Leech Hirudo medicinalis J Neurophysiol, July 1, 2005; 94(1): 441 - 453. [Abstract] [Full Text] [PDF]

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