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 ¿calculated 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.