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 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 μM 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. Received: 8 May 1997 / Received after revision: 31 July 1997 / Accepted: 19 August 1997