A lethal influx of extracellular calcium results from excitotoxicity, which happens when neurons are exposed to high levels of glutamate.
This results in a persistent activation of the N-methyl-d-aspartate acid (NMDA), -amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA), and voltage-gated calcium channels.
As cellular energy stores and Na+ gradients decline during hypoxia-ischemia, increased glutamate release and defective glutamate uptake create a toxic accumulation of extracellular glutamate, which causes glutamate receptors to become overstimulated and ultimately results in neuronal cell death.
Does excitotoxicity cause cell death?
Since excitotoxic stimulation of neurons may result in increased NO synthesis and exposure of neurons to NO may result in the release of excitotoxins, these two pathogenic mechanisms are intimately related. Excitotoxic neuronal death can be either apoptotic or necrotic, depending on the experimental conditions and cell type.
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