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Abstract
During ischemic brain injury, glutamate accumulation leads to overstimulation of postsynaptic
glutamate receptors with intracellular Ca2+ overload and neuronal cell death. Here
we show that glutamate can induce either early necrosis or delayed apoptosis in cultures
of cerebellar granule cells. During and shortly after exposure to glutamate, a subpopulation
of neurons died by necrosis. In these cells, mitochondrial membrane potential collapsed,
nuclei swelled, and intracellular debris were scattered in the incubation medium.
Neurons surviving the early necrotic phase recovered mitochondrial potential and energy
levels. Later, they underwent apoptosis, as shown by the formation of apoptotic nuclei
and by chromatin degradation into high and low molecular weight fragments. These results
suggest that mitochondrial function is a critical factor that determines the mode
of neuronal death in excitotoxicity.