Intracellular alkalinization causes Mg2+ release from intracellular binding sites in leech Retzius neurones

Four-barrelled ion-sensitive microelectrodes were developed to enable simultaneous measurement of intracellular free Mg2+ and Naf 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 mu M 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 pH(i). It is concluded that an intracellular alkalinization might induce the release of Mg2+ from intracellular stores.