ArticleJournal of neurochemistry2012
Bi-directional regulation of CaMKIIα phosphorylation at Thr286 by NMDA receptors in cultured cortical neurons.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- TargetingInternational journal of molecular sciences · 2024Review
- Roles of Phosphorylation of N-Methyl-D-Aspartate Receptor in Chronic Pain.Cellular and molecular neurobiology · 2023Review
- Investigating the role of CaNeural regeneration research · 2022Article
- Review
- Article
- Autophosphorylated CaMKII Facilitates Spike Propagation in Rat Optic Nerve.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Thalamo-cortical axons regulate the radial dispersion of neocortical GABAergic interneurons.eLife · 2016Article
- Capsaicin induces browning of white adipose tissue and counters obesity by activating TRPV1 channel-dependent mechanisms.British journal of pharmacology · 2016Article
- Basic roles of key molecules connected with NMDAR signaling pathway on regulating learning and memory and synaptic plasticity.Military Medical Research · 2016Review
- MiR-219 Protects Against Seizure in the Kainic Acid Model of Epilepsy.Molecular neurobiology · 2016Article
- Excitotoxic insult results in a long-lasting activation of CaMKIIα and mitochondrial damage in living hippocampal neurons.PloS one · 2015Article
- Involvement of the GluN2A and GluN2B subunits in synaptic and extrasynaptic N-methyl-D-aspartate receptor function and neuronal excitotoxicity.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
The N-methyl-D-aspartate (NMDA) receptor (NMDAR)-stimulated autophosphorylation of calmodulin-dependent kinase IIα at Thr286 may regulate many aspects of neuroplasticity. Here, we show that low NMDA concentration (20 μM) up-regulated Thr286 phosphorylation, and high concentration (100 μM) caused dephosphorylation. We next modulated the strength of NMDAR activation by manipulating NMDAR 2A subunit (NR2A) and NMDAR 2B subunit (NR2B), which represent the major NMDAR subtypes in forebrain regions. Pharmacological inhibition and molecular knockdown of NR2A or NR2B blocked 20 μM NMDA-induced phosphorylation. Conversely, over-expression of NR2A or NR2B enhanced phosphorylation by 20 μM NMDA. The 100 μM NMDA-induced dephosphorylation was suppressed by inhibition or knockdown of NR2A or NR2B, and enhanced by over-expression of NR2A or NR2B. Compared to NR2A, NR2B showed a higher impact on the NMDA-stimulated bi-directional regulation of Thr286 phosphorylation. We further found that activation of NR2A and NR2B by 100 μM NMDA-induced dephosphorylation through protein phosphatases (PP) that are inhibited by high concentration okadaic acid (1 μM), but not by PP2A and PP2B inhibitors. This novel function of NMDAR in dynamic regulation of calmodulin-dependent kinase IIα activity provides new evidence to support the current understanding that, depending on the degree of activation, NMDAR may lead to different and even opposing effects on intracellular signaling.
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Registered trials
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.