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Regulation of NMDA receptor Ca2+ signalling and synaptic plasticity
Open accessAbstract
NMDARs (N-methyl-D-aspartate receptors) are critical for synaptic function throughout the CNS (central nervous system). NMDAR-mediated Ca2+ influx is implicated in neuronal differentiation, neuronal migration, synaptogenesis, structural remodelling, long-lasting forms of synaptic plasticity and higher cognitive functions. NMDAR-mediated Ca2+ signalling in dendritic spines is not static, but can be remodelled in a cell- and synapse-specific manner by NMDAR subunit composition, protein kinases and neuronal activity during development and in response to sensory experience. Recent evidence indicates that Ca2+ permeability of neuronal NMDARs, NMDAR-mediated Ca2+ signalling in spines and induction of NMDAR-dependent LTP (long-term potentiation) at hippocampal Schaffer collateral–CA1 synapses are under control of the cAMP/PKA (protein kinase A) signalling cascade. Thus, by enhancing Ca2+ influx through NMDARs in spines, PKA can regulate the induction of LTP. An emerging concept is that activity-dependent regulation of NMDAR-mediated Ca2+ signalling by PKA and by extracellular signals that modulate cAMP or protein phosphatases at synaptic sites provides a dynamic and potentially powerful mechanism for bi-directional regulation of synaptic efficacy and remodelling.
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“CaMKII is vital in controlling NMDA receptor activity (Incontro et al., 2018), which also acts as a calcium channel (Lau et al., 2009).”
From APOE3 Christchurch modulates β-catenin/Wnt signaling in iPS cell-derived cerebral organoids from Alzheimer’s cases (2024) · cites this paper as Lau et al., 2009
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Metadata
- Authors
- Lau, C. G., Takeuchi, K., Rodenas-Ruano, A., Takayasu, Y., Murphy, J., Bennett, M. V. L., & Zukin, R. S.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Zukin, R. Suzanne
- Venue
- Biochemical Society Transactions
- Publisher
- Portland Press Ltd.
- Published
- 2009-11-19
- Volume
- 37
- Issue
- 6
- Pages
- 1369-1374
- ISSN
- 0300-5127 (ISSN-L)
- 1470-8752
- PMC
- PMC3501105
- OpenAlex
- W2022873534
- Cited by
- 138
- References
- 86
- Citations by year
- 2026: 13 · 2025: 14 · 2024: 11 · 2023: 11 · 2022: 15 · 2021: 13 · 2020: 9 · 2019: 9 · 2018: 3 · 2017: 7 · 2016: 4 · 2015: 3 · 2014: 7 · 2013: 4 · 2012: 5
- FWCI
- 2.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Society Transactions (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS-20752, R01NS020752)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- NMDA receptor, calcium signaling, synaptic plasticity, long-term potentiation, dendritic spines, cAMP/PKA signaling, protein kinase A, NMDA receptor subunit composition, calcium permeability, protein phosphatase, synaptic remodeling
- MeSH terms
- Animals, Calcium, Isoenzymes, Neuronal Plasticity, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Cyclic AMP-Dependent Protein Kinases, Calcium Signaling, Dendritic Spines
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