GRIA1 and schizophrenia: Furthermore, our data suggest that when the interaction between βSAP97 and GluA1 is disrupted, either by reducing βSAP97 expression or schizophrenia-related missense mutations in βSAP97’s PDZ2 domain, AMPARs are released from perisynaptic sites into the PSD causing a pathological increase in synaptic strength in DG granule neurons (Fig. 5k) that likely disrupts information processing in the dentate gyrus.