Cited by 357Neuroscience and Neuropharmacology ResearchGenetics and Neurodevelopmental DisordersAmino Acid Enzymes and Metabolism

Homeostatic plasticity and NMDA receptor trafficking

Pérez-Otaño, Isabel, Ehlers, Michael D.·2005·Trends in Neurosciences

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.

Integrity signals

Registry

Crossref · 10.1016/j.tins.2005.03.004

Cites

116 of 116 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Synaptic scaling protocols homeostatically regulate both the NMDA and AMPA component of glutamatergic synaptic currents, and the change in AMPA and NMDA currents are proportional at individual synapses.

    “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

  • In this model, Aβ accumulates along the endosomal/lysosomal pathway that leads to dysfunction of multivesicular bodies, causing impairment of the ubiquitin-proteasome system, which also controls the fate of NMDARs undergoing endocytic vesicular trafficking.

    “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”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Pérez-Otaño, I., & Ehlers, M. D.
Affiliations
Duke Medical Center (US)
Corresponding author
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.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review