Magnesium Inhibits Ischemia Induced Calcium Accumulation in Hilar Neurones: Possible Effect of Nmda-Receptor
Ischemic damage in the hippocampus is characterized by a selective vulnerability. Seventy-two hours following ischemia both irreversible morphological changes and excessive calcium accumulation can be demonstrated in CA-1 pyramidal cells (delayed neurone death). However, hilar neurons show rapid ischemic changes. Six hours following ischemia morphological damage can be demonstrated in hilar neurons, and recently we found excessive accumulation of calcium, 45 min following ischemia. Much evidence has accumulated, that Ca2+ plays a pivotal role in the pathogenesis of ischemic brain damage. Part of the ischemia induced calcium influx takes place via the N-methyl-D-aspartate (NMDA) receptor coupled, magnesium gated calcium conductance.