抄録
Magnesium has an important influence on the excitability and viability of central neurons. Removal of extracellular magnesium results in activation of the NMDA subtype of glutamate receptor followed by excitotoxic neuronal death. We have investigated the role of magnesium using cultured neurons from embryonic rat brain along with fluorescent dyes to report intracellular magnesium concentrations. Our studies showed that magnesium can enter neurons through NMDA receptors under the appropriate ionic conditions, and that elevation of intracellular magnesium results in neuronal death. The mechanism by which this injury occurs is unknown, although we are currently exploring the impact of elevated intracellular magnesium on the function of neuronal mitochondria. These studies also suggest the presence of a sodium-magnesium exchange mechanism responsible for removal of magnesium from the cytoplasm. Interestingly, several studies have reported that magnesium is lost from intracellular compartments that include both mitochondria and the cytoplasm in conditions associated with neuronal injury. The transport mechanisms responsible for magnesium loss are not known. Collectively, these studies demonstrate that intracellular magnesium is an important variable controlling neuronal viability, but it remains to be seen whether magnesium overload or magnesium loss is the critical parameter. [Jpn J Physiol 54 Suppl:S37 (2004)]
