ArticleNeuroscience bulletin2013
Synaptic non-GluN2B-containing NMDA receptors regulate tyrosine phosphorylation of GluN2B 1472 tyrosine site in rat brain slices.
Article in Neuroscience bulletin, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- The primate-specific peptide Y-P30 regulates morphological maturation of neocortical dendritic spines.PloS one · 2019Article
- Increased Src Family Kinase Activity Disrupts Excitatory Synaptic Transmission and Impairs Remote Fear Memory in Forebrain Shp2-Deficient Mice.Molecular neurobiology · 2017Article
- IGF-1-Involved Negative Feedback of NR2B NMDA Subunits Protects Cultured Hippocampal Neurons Against NMDA-Induced Excitotoxicity.Molecular neurobiology · 2017Article
- Higher levels of phosphorylated Y1472 on GluN2B subunits in the frontal cortex of aged mice are associated with good spatial reference memory, but not cognitive flexibility.Age (Dordrecht, Netherlands) · 2016Article
- Effects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus.Journal of neurodevelopmental disorders · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of N-methyl-D-aspartate receptors (NMDARs) mediates changes in the phosphorylation status of the glutamate receptors themselves. Previous studies have indicated that during synaptic activity, tyrosine kinases (Src and Fyn) or phosphatases (PTPα and STEP) are involved in regulating the phosphorylation of NMDARs. In this study, we used immunoblotting to investigate the role of an NMDAR subpopulation on the phosphorylation level of the GluN2B subunit at the Y1336 and Y1472 sites in rat brain slices after NMDA treatment. We found that NMDA stimulation dramatically decreased the phosphorylation level of GluN2B at Y1472 in a dose- and time-dependent manner, but not at Y1336. Extrasynaptic NMDAR activation did not reduce the phosphorylation of GluN2B at Y1472. In addition, ifenprodil, a selective antagonist of GluN2B-containing NMDARs, did not abolish the decreased phosphorylation of GluN2B at Y1472 triggered by NMDA. These results suggest that the activation of synaptic GluN2A-containing NMDARs is required for the decreased phosphorylation of GluN2B at Y1472 that is induced by NMDA treatment in rat brain slices.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.