Topic: GluN1-C744Y

AIMS: Investigate the impact of disrupting specific disulfide bonds in the GluN1 subunit on the early trafficking and functional properties of conventional NMDARs.METHODS:HEK293 cells were utilized to express wild-type (WT) or mutant forms of GluN1/GluN2A and GluN1/GluN2B receptors. Surface expression and colocalization of NMDAR with the Golgi apparatus were observed using fluorescence confocal microscopy. Electrophysiological properties of NMDARs were assessed via the whole-cell patch-clamp technique. In addition, NMDA-induced excitotoxicity in rat hippocampal neurons was examined specificall

AIMS: Investigate the impact of disrupting specific disulfide bonds in the GluN1 subunit on the early trafficking and functional properties of unconventional NMDARs.METHODS:HEK293 cells and rat hippocampal neurons were used to express wild-type (WT) or mutant forms of GluN1/GluN3A receptors. Surface expression and colocalization of NMDARs with the Golgi apparatus (GA) were observed using fluorescence confocal microscopy. Electrophysiological properties of NMDARs were assessed via patch-clamp technique.RESULTS:Disrupting disulfide bonds in the GluN1 subunit co-transfected with GluN3A subunit le