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This should be a control of the release of glutamate in the synaptic cleft from presynaptic terminals to stimulate post-synaptic neurons (i.e., the NMDA receptors) and re-uptake from the cleft by the excitatory amino acid transporters (EAAT) into astrocytes, and glutamate/glutamine cycle within astrocytes [59]

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[DOI] [PubMed] [Google Scholar] Redorta J