Glutamate is the primary excitatory neurotransmitter in the brain. The cycle of glutamate synthesis, release, and reuptake is tightly linked to glucose metabolism. In the setting of ischemia, this cycle is disrupted: Glutamate release is increased and uptake is impaired, leading to pathologic prolonged stimulation of glutamate receptors (including the NMDA receptor) and neuronal cell death—a process called "excitotoxicity" (25). Compared to that in the adult brain, the NMDA receptor in the newborn brain is more highly expressed, has a higher affinity for glutamate, and is more active (26-28). These developmental differences render the immature brain more susceptible to excitotoxicity (29). In fact, it has been reported that exposure of the neonatal rat brain to treatments aimed at reducing excitotoxicity by targeting the NMDA receptor, even in a normal brain, accelerates programmed cell death (30). This paradoxic effect probably relates to developmental differences in glutamate signaling, as well as innate programmed cell death occurring during this period (see below).

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