Intracellular Mg2+ regulation in voltage‐clamped Helix aspersa neurones measured with mag‐fura‐2 and Mg(2+)‐sensitive microelectrodes

The extrusion mechanism for intracellular Mg2+ was investigated in voltage‐clamped snail neurones using Mg(2+)‐sensitive microelectrodes and mag‐fura‐2. The intracellular free magnesium ion concentration ([Mg2+]1) of snail neurones voltage clamped to ‐60 mV was estimated to be 0.57 +/− 0.06 mM (mean +/− S.E.M.; n = 12) using Mg(2+)‐sensitive microelectrodes and 0.62 +/− 0.05 mM (n = 15) using mag‐fura‐2. Raising extracellular MgCl2 from 5 to 20 mM caused an average increase in [Mg2+]1 of 0.25 +/− 0.04 mM (n = 7). In three experiments, removing extracellular Mg Cl2 caused an average decrease in [Mg2+]1 of 0.1 mM. Replacing extracellular Na+ with N‐methyl‐D‐glucamine (NMDG) caused a rise in [Mg2+]1 of 1.8 +/− 0.5 mM (n = 7); [Mg2+]1 recovered to resting levels when extracellular Na+ was restored. Iontophoretic injections of MgCl2 were used to raise [Mg2+]1. The rate of recovery from such increases in [Mg2+]1 inverted question markcalculated from the slope of the recovery was inhibited by 85‐100% (n = 5) in the absence of extracellular Na2+ compared with control conditions. Raising extracellular Ca2+ from 7 to 35 mM caused a reversible rise in [Mg 2+]1 of 0.4 +/− 0.05 mM (mean +/− S.E.M., n = 7). It was concluded that in snail neurones the main mechanism for [Mg2+]1 extrusion is a Na(+)‐Mg2+ exchanger which may be partially inhibited be high extracellular Ca2+ concentrations.