Figure 1

PSD-95 deficiency alters specific AMPAR and NMDAR-subunit protein expression levels in the mPFC at postnatal day 35, but not postnatal day 21. (A) Left panel shows representative blots for AMPAR subunits (GluA1 & GluA2) and NMDAR subunits (GluN1, GluN2A, GluN2B, and GluN3A) in control (Con) versus PSD-95 knockout (KO) mice at P21. All proteins were normalized to actin. Right panel displays summary graphs of protein expression levels in arbitrary units (a.u.) of GluA1 (p = 0.28, Con, n = 7, KO, n = 8), GluA2 (p = 0.39, n = 6), GluN1 (p = 0.23, Con, n = 7, KO, n = 10), GluN2A (p = 0.85, Con, n = 8, KO, n = 10), GluN2B (p = 0.51, Con, n = 7, KO, n = 10), GluN3A (p = 0.15, Con, n = 8, KO, n = 9) in Con vs. KO mice. (B) Left panel shows representative blots for AMPAR subunits, NMDAR subunits and actin at P35 in con vs. KO mice. Right panel displays summary graphs of protein expression levels in a.u. in GluA1 (p = 0.04, n = 7), GluA2 (p = 0.51, Con, n = 8, KO, n = 5) GluN1 (p = 0.002, Con, n = 10, KO, n = 8); GluN2A (p = 0.18, Con, n = 9, KO, n = 8) GluN2B (p = 0.02, n = 7), GluN3A (p = 0.08, Con, n = 9, KO, n = 8) in Con vs. KO mice. PSD-95 deficiency causes a significant increase in SAP-102 that leads to an increase in interaction of GluN2B in the mPFC. (C) Upper panel shows representative western blots of SAP-102 and PSD-93 in control versus PSD-95 knockout mice. Both proteins were normalized to actin. Lower panel displays summary graphs of protein expression levels of SAP-102 and PSD-93 in Con vs. KO mice (SAP-102, p = 9 × 10⁻⁷, n = 7; PSD-93, p = 3 × 10⁻⁶, Con, n = 7, KO, n = 6). (D) Upper panel shows blots of SAP-102 and GluN2B co-immunoprecipitation in Con vs. KO mice. GluA1 was used as a negative control. Lower panel displays a summary graph of protein levels of GluN2B and SAP-102 interaction (GluN2B/SAP-102, p = 0.03, n = 5). All full length/uncropped western blots are presented in Supplementary Fig. 2. *p < 0.05, **p < 0.01, ****p < 0.0001, n.s., not significant.