title: Intracellular alkalinization causes Mg2+ release from intracellular binding sites in leech Retzius neurones.
abstract: Four-barrelled ion-sensitive microelectrodes were developed to enable simultaneous measurement of intracellular free Mg2+ and Na+ concentrations ([Mg2+]i, [Na+]i), intracellular pH and the membrane potential. The electrodes were used to investigate pH-induced [Mg2+]i changes in Retzius neurones of the leech Hirudo medicinalis. The application of propionate or CO2/HCO3--buffered bath solutions caused a transient intracellular acidification, an initial [Mg2+]i decrease and a continuous [Na+]i increase. In the presence of CO2/HCO3- this [Na+]i increase was more pronounced and might be the reason for the slow increase in [Mg2+]i following the initial decrease. The withdrawal of propionate or CO2/HCO3--buffered bath solutions caused a transient alkalinization which was accompanied by a slight but significant [Mg2+]i increase, even in the nominal absence of extracellular Mg2+, while [Na+]i returned to its original value. The alkalinization-induced [Mg2+]i increase could be reduced to about 50% by the application of 1-10 microM cyclosporin A, an inhibitor of the mitochondrial permeability transition pore (MTP). Phenylarsine oxide, an MTP activator, caused a [Mg2+]i increase with characteristics similar to those of the alkalinization-induced increase, which could not be attributed to any changes in [Na+]i or pHi. It is concluded that an intracellular alkalinization might induce the release of Mg2+ from intracellular stores.
authors.affiliation: Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Universitätsstrasse 1, D-40225 Düsseldorf, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Günzel
authors.forename: S
authors.initials: S
authors.lastname: Durry
authors.forename: W R
authors.initials: WR
authors.lastname: Schlue
mesh_terms: D000818:Animals; D001152:Arsenicals / Q000494:pharmacology; D001639:Bicarbonates / Q000008:administration & dosage / Q000494:pharmacology; D001665:Binding Sites; D002021:Buffers; D002245:Carbon Dioxide / Q000008:administration & dosage / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D007865:Leeches / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism*; D008564:Membrane Potentials; D008839:Microelectrodes; D009474:Neurons / Q000378:metabolism*; D011422:Propionates / Q000008:administration & dosage / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism
chemical_list: D001152:Arsenicals; D001639:Bicarbonates; D002021:Buffers; D011422:Propionates; C029341:oxophenylarsine; D002245:Carbon Dioxide; D016572:Cyclosporine; D012964:Sodium; D008274:Magnesium; C029658:propionic acid