SLC1A2 and schizophrenia: Reduced perisynaptic glutamate buffering, leading to glutamate spillover and loss of signaling specificity are molecular features implicated in schizophrenia pathophysiology.2,37 As the N-glycosylation status of EAAT1 and EAAT2 regulates their expression in the plasma membrane,38 smaller N-glycans on these molecules may contribute to glutamatergic signaling alterations in this illness by impacting the ability of astroglia to modulate extracellular glutamate levels.28,37,39