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A summary of the pathophysiology of HIE is presented graphically. Glutamate (GLU) is packaged into vesicles in the presynaptic terminal. Upon
depolarization, glutamate is released into the neurosynaptic junction and binds to glutamate receptors on the postsynaptic dendrite. Binding to the kainate
(KA) and AMPA receptors triggers the influx of sodium (Na), resulting in the depolarization of the postsynaptic neuron. Binding to NMDA receptors triggers
the influx of calcium and sodium into the postsynaptic dendrite. Glutamate is then removed from the neurosynaptic junction via the excitatory amino acid
transporters (EAATs) located on the atrocyte. It is then converted into glutamine by the enzyme glutamine synthetase. The glutamine is exported from the
astrocyte into the presynaptic neuron, and then converted into glutamate via the action of glutaminase, thus recycling the neurotransmitter. This process is
Source: Chapter 28. Newborn Neurology, Pediatric Practice: Neurology
known as the glutamine–glutamate cycle (shown in yellow). During HIE, there is a massive release of the excitatory amino acid glutamate from the
Citation: This
Carney
PR,toGeyer
JD. Pediatric
Practice:
Neurology;
2010
Available
http://mhmedical.com/
Accessed:neuron,
May 13,leading
2017 to neuronal
presynaptic terminal.
leads
overstimulation
of the
glutamate
receptors
(AMPA,
KA, at:
NMDA)
located on the postsynaptic
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death, a process termed excitotoxicity. Overstimulation of the KA and AMPA receptors leads to the entry of sodium and chloride into the cell, which
increases cell osmality. The increased influx of sodiums leads to the influx of water, which results in subcellular edema, which if severe enough results in
lysis of the cell. Overstimulation of the NMDA receptor triggers the influx of calcium (green). In addition, calcium also enters via the voltage-dependent