Cited by 138Neuroscience and Neuropharmacology ResearchTreatment of Major DepressionAmino Acid Enzymes and Metabolism

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Regulation of NMDA receptor Ca2+ signalling and synaptic plasticity

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Lau, C. Geoffrey, Takeuchi, Koichi, Rodenas-Ruano, Alma, Takayasu, Yukihiro, Murphy, Jessica, Bennett, Michael V.L., Zukin, R. Suzanne·2009·Biochemical Society Transactions

DOI 10.1042/bst0371369PMC PMC3501105

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Abstract

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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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
ORCID: Lau, C. Geoffrey
Rodenas-Ruano, Alma
Takayasu, Yukihiro
Bennett, Michael V.L.
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
DOI: 10.1042/bst0371369
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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Regulation of NMDA receptor Ca2+ signalling and synaptic plasticity

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