Journal: Translational Psychiatry
Article Title: Alteration of NMDA receptor trafficking as a cellular hallmark of psychosis
Figure Lengend Snippet: Cerebrospinal fluid (CSF) from patients with SCZSD alters the surface dynamics of synaptic NMDAR. a Schematic description of the experimental workflow. CSF from patients with schizophrenic spectrum disorders (SCZSD, n = 12), affective spectrum disorders (AffectSD, n = 9) subarachnoid hemorrhage (SAH, n = 9 patients), brain polytrauma ( n = 3), hemophagocytic lymphohistiocytosis (HLH, n = 1), were collected. Then, single nanoparticle (QDot) tracking of GluN2B-NMDAR was performed onto cultured hippocampal neurons exposed to CSF. b Representative trajectories (50 ms acquisition) of surface GluN2B-NMDAR-QD complexes in dendritic spines of neurons exposed to various CSFs. Scale bar = 300 nm. c Diffusion coefficient (µm 2 /s) of synaptic GluN2B-NMDAR values after exposure for 15–30 min to patients’ CSF. Each plotted dot corresponds to the median diffusion coefficient value of one patient CSF. The mean and standard deviation (SD) are represented for each condition. Right panel , Comparison of GluN2B-NMDAR synaptic diffusion coefficient values after exposure for 15–30 min to patients’ CSF (Control, n = 2757 trajectories; SCZSD, n = 5849; AffectSD, n = 2410; Polytrauma, n = 825; SAB, n = 3957; *** p
Article Snippet: Endogenous surface GluN2B-NMDAR or transfected GluN2A-SEP, GluN3A-SEP, GluA1-SEP, GABA-gamma2-GFP, or Dopamine D1-YFP were immune stained in live neurons using a rabbit polyclonal anti-GluN2B (1:200; Alomone, Israel) or mouse monoclonal anti-GFP (1:500, Roche, Switzerland), respectively.
Techniques: Cell Culture, Diffusion-based Assay, Standard Deviation