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Homeostatic plasticity and NMDA receptor trafficking
Abstract
Learning, memory and brain development are associated with long-lasting modifications of synapses that are guided by specific patterns of neuronal activity. Such modifications include classical Hebbian plasticities (such as long-term potentiation and long-term depression), which are rapid and synapse-specific, and others, such as synaptic scaling and metaplasticity, that work over longer timescales and are crucial for maintaining and orchestrating neuronal network function. The cellular mechanisms underlying Hebbian plasticity have been well studied and involve rapid changes in the trafficking of highly mobile AMPA receptors. An emerging concept is that activity-dependent alterations in NMDA receptor trafficking contribute to homeostatic plasticity at central glutamatergic synapses.
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“Interestingly, synaptic scaling protocols homeostatically regulate both the NMDA and the AMPA component of glutamatergic synaptic currents, and the change in AMPA and NMDA currents are proportional at individual synapses (Watt et al. 2000;Perez-Otano and Ehlers 2005).”
From Homeostatic Synaptic Plasticity: Local and Global Mechanisms for Stabilizing Neuronal Function (2012) · cites this paper as Perez-Otano and Ehlers 2005
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“In this model, Ab accumulates along the endosomal/lysomal pathway that leads to dysfunction of multivesicular bodies, causing impairment of the ubiquitin-proteasome system, 9 which also controls the fate of NMDARs undergoing endocytic vesicular trafficking.50”
From Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration (2013) · cites this paper as [50]
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Metadata
- Authors
- Pérez-Otaño, I., & Ehlers, M. D.
- Affiliations
- Duke Medical Center (US)
- Corresponding author
- Ehlers, Michael D.
- ORCID
- Ehlers, Michael D.
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 28
- Issue
- 5
- Pages
- 229-238
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W2020939800
- Cited by
- 356
- References
- 116
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 4 · 2022: 4 · 2021: 11 · 2020: 11 · 2019: 16 · 2018: 7 · 2017: 12 · 2016: 10 · 2015: 13 · 2014: 14 · 2013: 25 · 2012: 22
- FWCI
- 3.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Mental Health (R01MH064748, MH 64748)
- National Institute of Neurological Disorders and Stroke (NS 39402, R01NS039402, NS 32742)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Keywords
- homeostatic plasticity, NMDA receptor trafficking, synaptic scaling, metaplasticity, Hebbian plasticity, long-term potentiation, long-term depression, AMPA receptor trafficking, glutamatergic synapses, activity-dependent synaptic plasticity
- MeSH terms
- Animals, Homeostasis, Humans, Neuronal Plasticity, Receptors, N-Methyl-D-Aspartate, Protein Transport
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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