ReviewMolecular neurobiology2011
Regulation of long-term plasticity induction by the channel and C-terminal domains of GluN2 subunits.
Review in Molecular neurobiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Individual NMDA receptor GluN2 subunit signaling domains differentially regulate the postnatal maturation of hippocampal excitatory synaptic transmission and plasticity but not dendritic morphology.Synapse (New York, N.Y.) · 2024Article
- Stress enhances expression of calcium-binding proteins and NMDAR subunit genes in the rat hippocampus.Neuroprotection (Chichester, England) · 2024Article
- Targeting NMDA Receptors in Emotional Disorders: Their Role in Neuroprotection.Brain sciences · 2022Review
- Mechanism of Oxidative Stress and Synapse Dysfunction in the Pathogenesis of Alzheimer's Disease: Understanding the Therapeutics Strategies.Molecular neurobiology · 2016Review
- GRIN2B predicts attention problems among disadvantaged children.European child & adolescent psychiatry · 2015Article
- Association of genetic variants of GRIN2B with autism.Scientific reports · 2015Article
- Developmental vulnerability of synapses and circuits associated with neuropsychiatric disorders.Journal of neurochemistry · 2013Review
- Dynamic regulation of NMDAR function in the adult brain by the stress hormone corticosterone.Frontiers in cellular neuroscience · 2012Article
- Article
- Dual impact of neuroinflammation on cognitive and motor impairments in Alzheimer's disease.Journal of Alzheimer's disease reportsReview
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conventional long-term potentiation (LTP) and long-term depression (LTD) are induced by different patterns of synaptic stimulation, but both forms of synaptic modification require calcium influx through NMDA receptors (NMDARs). A prevailing model (the "calcium hypothesis") suggests that high postsynaptic calcium elevation results in LTP, whereas moderate elevations give rise to LTD. Recently, additional evidence has come to suggest that differential activation of NMDAR subunits also factors in determining which type of plasticity is induced. While the growing amount of data suggest that activation of NMDARs containing specific GluN2 subunits plays an important role in the induction of plasticity, it remains less clear which subunit is tied to which form of plasticity. Additionally, it remains to be determined which properties of the subunits confer upon them the ability to differentially induce long-term plasticity. This review highlights recent studies suggesting differential roles for the subunits, as well as findings that begin to shed light on how two similar subunits may be linked to the induction of opposing forms of plasticity.
Indexed as
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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.