Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 333K) PPT slides of all figures Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JGP Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Müller, A. Articles by Schlue, W.-R. Search for Related Content PubMed PubMed Citation Articles by Müller, A. Articles by Schlue, W.-R. Social Bookmarking                      What's this?

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

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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]

Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents