PubMed · 1990 · 43 citations · 0 references
MedicineNeurosciencePharmacologyCellular NeuroscienceNeurochemistryNeuropharmacologyAcute Ischemic StrokeNeuroprotectionNeuroprotective PharmacologyNeurotransmissionStrokeCerebral Ischemia NeuroprotectionCerebral Ischemia PharmacotherapyExcitatory Pyramidal NeuronsGlutamate AntagonistsGlutamatergic NeuroprotectionGlutamatergic SynapsesIschemic Neuronal DeathNeural Ischemia
The hippocampal lesion induced by cerebral ischemia has several excitotoxic features. Denervation of the ischemia-vulnerable pyramidal cells has a protective effect. Because most synapses are glutamatergic, administration of glutamate antagonists after ischemia also could be protective. Growing evidence now indicates that non-N-methyl-D-aspartate antagonists are more effective than N-methyl-D-aspartate antagonists in complete global ischemia. One explanation offered is that ischemia may sensitize pyramidal neurons so that "normal" postischemic synaptic activity induces lethal damage.