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Sodium- and chloride-dependent glycine transporter 1 (GlyT1) is a transmembrane protein encoded by the SLC6A9 gene and predominantly expressed in glial cells and at glutamatergic synapses in the central nervous system[6][5][7]. GlyT1 is essential for tightly regulating extracellular glycine concentrations at inhibitory glycinergic synapses and for modulating NMDA receptor activation, where glycine acts as a necessary co-agonist[5][1]. By controlling synaptic glycine, GlyT1 modulates glutamatergic neurotransmission and influences cognitive functions. Dysregulation or mutation of GlyT1 can result in neurological disorders such as glycine encephalopathy[6]. GlyT1 inhibitors, such as bitopertin and iclepertin, have been clinically explored to enhance cognitive function in schizophrenia and related disorders by increasing glycine levels and thereby strengthening NMDA receptor-mediated neurotransmission[6][4].
Inhibition increases synaptic glycine levels and potentiates NMDA receptor function, Enhancement of cognitive function via NMDA receptor modulation
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