glun2d subunit  (Alomone Labs)

Journal: British Journal of Pharmacology

Article Title: Ketamine and phencyclidine: the good, the bad and the unexpected

doi: 10.1111/bph.13222

Figure Lengend Snippet: Tables of Links

Article Snippet: [ PubMed ] Yamamoto H, Kamegaya E, Sawada W, Hasegawa R, Yamamoto T, Hagino Y, et al. Involvement of the N-methyl-D-aspartate receptor GluN2D subunit in phencyclidine-induced motor impairment, gene expression, and increased Fos immunoreactivity.

Techniques:

Journal: The Journal of Neuroscience

Article Title: GluN2D Subunit-Containing NMDA Receptors Control Tissue Plasminogen Activator-Mediated Spatial Memory

doi: 10.1523/JNEUROSCI.6202-11.2012

Figure Lengend Snippet: Active immunization selectively prevents tPA/GluN1 interaction and tPA-induced enhancement of NMDAR signaling without altering the basal Ca2+ conductivity. A, Schematic representation of NMDAR composed of GluN1/GluN2D subunits, including binding sites of αATD–GluN1, αCTD–GluN1, and αCTD–GluN2D antibodies, UBP145, and tPA. B, ATD–GluN1 immunized mice display antibodies specifically targeting the GluN1 subunit of NMDAR. Proteins extracts from naive mouse brain (n = 3) were subjected to immunoblots revealed with IgGs purified from either control mice (control IgGs) or ATD–GluN1 (120 kDa) immunized mice (αATD–GluN1). Parallel immunoblottings were performed and revealed with antibodies raised against either CTD–GluN1 (named αCTD–GluN1), known to reveal a band at ∼120 kDa, or CTD–GluN2D (named αCTD–GluN2D), known to reveal a band at ∼165 kDa. C, After immunization, mice display circulating antibodies against GluN1, capable of preventing the potentiating effect of tPA on GluN1/GluN2D subunit-containing NMDARs. NMDA induces Ca2+ influx in cortical neurons as measured by fura-2 video microscopy (N = 3, n = 150 cells). Coapplication of tPA (20 μg/ml; 45 min) potentiates the NMDA-evoked Ca2+ influx by 47% (N = 3, n = 108 cells). Neither UBP145 alone (0.2 μm; N = 3, n = 150 cells) nor αATD–GluN1 antibodies alone (0.01 mg/ml; N = 3, n = 108 cells) alter NMDA-induced Ca2+ influx. Both UBP145 (0.2 μm) and αATD–GluN1 (0.01 mg/ml) are capable of blocking this potentiating effect of tPA (N = 3, n = 150 cells and N = 3, n = 108 cells, respectively). Ctrl, Control; HBBSS, serum-free medium. Paired Student's t test (before vs after treatment), *p < 0.001. Vertical bars indicate SD.

Article Snippet: Subjects Homozygous male mutant mice lacking the GluN2D subunit of NMDAR were generated by Prof. Mishina (University of Tokyo, Tokyo, Japan) ( Ikeda et al., 1995 ) and provided by the RIKEN BioResource Center.

Techniques: Binding Assay, Western Blot, Purification, Control, Microscopy, Blocking Assay

Journal: The Journal of Neuroscience

Article Title: GluN2D Subunit-Containing NMDA Receptors Control Tissue Plasminogen Activator-Mediated Spatial Memory

doi: 10.1523/JNEUROSCI.6202-11.2012

Figure Lengend Snippet: Regulation of NMDAR subunits (GluN1, GluN2A, GluN2B, GluN2D) in hippocampus after active immunization against the ATD of the NMDAR GluN1 subunit. Relative mRNA quantity, estimated by RT-qPCR, was expressed in 2−(Ct gene of interest), in which Ct is the threshold cycle value. A, GluN1 subunit mRNA expression. B, GluN2A subunit mRNA expression. C, GluN2B subunit mRNA expression. D, GluN2D subunit mRNA expression. WT Crude ATD mice, n = 5; WT Crude Control mice, n = 5. Mann–Whitney U test, *p < 0.05. Vertical bars indicate SD.

Article Snippet: Subjects Homozygous male mutant mice lacking the GluN2D subunit of NMDAR were generated by Prof. Mishina (University of Tokyo, Tokyo, Japan) ( Ikeda et al., 1995 ) and provided by the RIKEN BioResource Center.

Techniques: Quantitative RT-PCR, Expressing, Control, MANN-WHITNEY

Journal: The Journal of Neuroscience

Article Title: GluN2D Subunit-Containing NMDA Receptors Control Tissue Plasminogen Activator-Mediated Spatial Memory

doi: 10.1523/JNEUROSCI.6202-11.2012

Figure Lengend Snippet: GluN1/GluN2D subunit-containing NMDARs drive tPA-influenced spatial memory. A, Previous studies have evidenced that tPA was not involved in locomotor activity (Pawlak et al., 2002). However, tPA is known to influence both emotional (Calabresi et al., 2000) and spatial memories (Benchenane et al., 2007). B, Our present experiments reveal that inhibition of the tPA/NMDAR interaction prevents neither locomotor activity nor emotional memory in mice. In addition, our results show that the tPA/NMDAR interaction is a critical mechanism underlying tPA-influenced spatial memory. C, In agreement with Ikeda et al. (1995), we observe a decrease in spontaneous locomotor activity in GluN2D-deficient mice. Furthermore, our present study reveals impairments of both emotional and spatial memories in this strain. In addition, we also show that the inhibition of tPA/NMDAR interaction does not impair the spatial memory in GluN2D KO mice. Together, these results demonstrate that tPA influences spatial memory through an increased affinity for NMDAR when associated with GluN2D subunit. Arrows point to the behavioral deficit.

Article Snippet: Subjects Homozygous male mutant mice lacking the GluN2D subunit of NMDAR were generated by Prof. Mishina (University of Tokyo, Tokyo, Japan) ( Ikeda et al., 1995 ) and provided by the RIKEN BioResource Center.

Techniques: Activity Assay, Inhibition