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The proposed mechanism involves controlling glutamate release in the synaptic cleft, modulating NMDA receptor stimulation, affecting excitatory amino acid transporter (EAAT)-mediated reuptake, and maintaining the glutamate/glutamine cycle within astrocytes
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in the Surgical Forum (1985)
Additionally, elevated SAMe (from over-supplementation) may increase glutamatergic tone, further exacerbating the excitatory/inhibitory imbalance already present in CIRS terrain
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