Glun2a, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
Average 95 stars, based on 7 article reviews
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1) Product Images from "Surface dynamics of GluN2B-NMDA receptors controls plasticity of maturing glutamate synapses"
Article Title: Surface dynamics of GluN2B-NMDA receptors controls plasticity of maturing glutamate synapses
Journal: The EMBO Journal
Figure Legend Snippet: Synaptic GluN2B-NMDAR are laterally redistributed in the synaptic area following chem LTP in immature neurons Detection of a single QD (30-Hz acquisition) in our experimental conditions. The high signal-to-noise ratio (SNR) ( > 5) enables the detection and location of the signal with a high pointing accuracy (˜30 nm). The QD fluorescence is quantified on a pseudocolor scale (low: red; high: yellow). Scale bar = 800 nm. A 500-frame stack is obtained while tracking down a single NMDAR/QD complex. On each frame, a single GluN2B- (green) or GluN2A- (blue) QD particle complex is detected and precisely located within synaptic (dark gray) and perisynaptic (320-nm annulus around the synapse; light gray) areas. Those 500 locations are then projected on a single image, providing the successive positions of this receptor/particle complex during the 500-frame stack. Note that GluN2A-NMDAR are more concentrated within the core of the PSD. Scale bar image = 300 nm; synaptic areas = 200 nm. Relative fraction of synaptic and perisynaptic GluN2-QD particles, calculated before and after chem LTP for both GluN2B- (left) and GluN2A-NMDAR (right) ( n = 25 and 20 dendritic fields before and after chem LTP, respectively). Note the significant decrease in the relative synaptic content in GluN2B-NMDAR particles right after chem LTP (Student's t -test, ** P
Techniques Used: Fluorescence
2) Product Images from "Human endogenous retroviral protein triggers deficit in glutamate synapse maturation and behaviors associated with psychosis"
Article Title: Human endogenous retroviral protein triggers deficit in glutamate synapse maturation and behaviors associated with psychosis
Journal: Science Advances
Figure Legend Snippet: Recombinant Env disperses synaptic NMDAR in hippocampal neurons without interfering with the ionotropic function. ( A ) Experimental setup of (yellow) neurons [microtubule-associated protein 2 (MAP-2) positive] and (magenta) glia [glial fibrillary acidic protein (GFAP) and Iba1 positive]. Representative NMDAR-mediated Ca 2+ signals and detected transients (dots) 5 min after Cont. (vehicle) or Env exposure. Scale bars, 30 and 1 μm. ( B ) Ca 2+ frequency ratio (post/pre) for blank ( n = 47/5 spines/neurons); Cont. ( n = 92/7); and Env: 0.5 μg/ml ( n = 87/6), 1.0 μg/ml ( n = 114/9), and 10 μg/ml ( n = 18/1). ( C ) Representative NMDA traces and mean peak amplitudes before (pre) and 5 min after (post) Cont. or Env application. ( D ) Representative trajectories of GluN2A- and GluN2B-NMDAR-QD complexes at postsynaptic densities (PSD). Scale bar, 1 μm. ( E ) Synaptic increase of GluN2B-NMDAR but not GluN2A-NMDAR surface diffusion. Data are normalized to pre-exposure for individual neurons. GluN2A, Cont. (vehicle; n = 176/4 trajectories/neuron) and Env ( n = 200/5). GluN2B, Cont. ( n = 670/16) and Env ( n = 792/17). *** P
Techniques Used: Recombinant, Diffusion-based Assay
Figure Legend Snippet: Neonatal Env expression tunes glutamatergic synapse maturation and is necessary for psychotic-like behavior. ( A ) Subcellular fractionation of hippocampal tissue. Note the enrichment of NMDA receptors (represented by GluN2A) and postsynaptic density proteins (PSD-95) in P2 and synaptosome (synaptic proteins enriched) fractions compared to initial homogenate and the depletion of glia (GFAP) in the same. ( B ) Representative images of inserted gene distribution at P7. Scale bars, 1 mm. ( C ) Hippocampal inserted gene expression at ~P65. ( D ) Env exposure tends to influence GluN2A/PSD-95 subunit stabilization in the synapse (P7; Cont. versus Env; P = 0.06) that then remains constant. Interaction: F (1,29) = 8.69, two-way ANOVA and Bonferroni's multiple comparisons test; * P = 0.021 and *** P = 0.0004. ( E ) GluN2B/PSD-95 expression is unaffected by Env at both ages. Interaction: F (1,29) = 2.46, P = 0.13, two-way ANOVA and Bonferroni's multiple comparisons test; *** P
Techniques Used: Expressing, Fractionation
3) Product Images from "Cholesterol modulates presynaptic and postsynaptic properties of excitatory synaptic transmission"
Article Title: Cholesterol modulates presynaptic and postsynaptic properties of excitatory synaptic transmission
Journal: Scientific Reports
Figure Legend Snippet: Cholesterol depletion reduces synaptic localization of NMDARs. ( A , C ) Colocalization of surface GluN2A (A, green) or GluN2B (C, green) and the postsynaptic marker Shank (red) in control and cholesterol-depleted neurons (10 mM MβCD pretreatment, 5 min). Scale bar 2 µm. ( B , D ) Bar graphs showing Pearson's coefficient for the colocalization indicate the reduction of synaptic localization of GluN2A and GluN2B after cholesterol depletion. ( E ) Colocalization of surface GluA1 (green) and the postsynaptic marker Shank (red) in control and cholesterol-depleted neurons (MβCD). Scale bar 2 µm. ( F ) Bar graph showing Pearson's coefficient for the colocalization. ( G ) Examples of typical dual AMPAR-NMDAR mEPSCs in control autaptic neurons having various AMPAR to NMDAR ratio. ( H ) Examples of typical dual AMPAR-NMDAR mEPSCs in 10 mM MβCD-pretreated autaptic neurons. ( I ) Examples of NMDAR mEPSCs obtained from average dual mEPSCs after AMPAR mEPSC subtraction. A control neuron (top trace) and a cholesterol-depleted neuron (bottom trace). The arrows indicate mEPSC onsets. ( J ) The comparison of average amplitude of NMDAR mEPSCs in control neurons and in cholesterol-depleted neurons. (* p
Techniques Used: Marker
Figure Legend Snippet: Cholesterol depletion reduces the fraction of synaptic immobile NMDARs. ( A ) Surface NMDARs were detected using a QD-antibody complex directed against extracellular epitopes in GluN2A or GluN2B. Left, representative summed trajectories of NMDAR-QDs (red) acquired over a period of 25 s (20 Hz frame rate) in hippocampal neurons. Scale bar 5 µm. Right, representative examples of NMDAR reconstructed trajectories. ( B , C ) Diffusion coefficients for synaptic GluN2A-containing NMDARs and GluN2B-containing NMDARs in control and after cholesterol depletion (10 mM MβCD pretreatment, 5 min). ( D , E ) Diffusion coefficients for extrasynaptic GluN2A-containing NMDAR and GluN2B-containing NMDARs in control and after cholesterol depletion. ( F , G ) Diffusion coefficients for the mobile fraction of synaptic GluN2A and GluN2B-containing NMDARs in control and after cholesterol depletion. ( H , I ) Fraction of synaptic immobile receptors in control and after cholesterol depletion. (* p
Techniques Used: Diffusion-based Assay