EAAT1 and EAAT2, which modulate glutamate uptake from the synaptic cleft and extrasynaptic extracellular matrix into astroglia, are abnormally N-glycosylated in schizophrenia anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex (DLPFC), respectively.28 In the ACC, the EAAT1 monomer demonstrates a smaller shift after PNGaseF treatment, indicating that EAAT1 N-glycans are of smaller molecular mass in schizophrenia, whereas EAAT2 demonstrates a reduced PNGaseF shift of its multimeric form in the DLPFC in schizophrenia. Here, SLC1A3 is linked to schizophrenia.