Neuronal protection with magnesium.

Delayed neuronal death following hypoxic ischaemic insult is primarily mediated by the N-methyl D-aspartate (NMDA) receptor. The NMDA receptor antagonist MK 801, has been shown to limit neuronal death following hypoxic ischaemic injury but is too toxic to be used in the human neonate. Magnesium blocks the NMDA channel in a voltage dependent manner. Its administration after a simulated hypoxic ischaemic insult limits neurological damage in several animal models. The efficacy of magnesium in providing neuroprotection in the human neonate, however needs to be established in controlled clinical trials.