Cited by 223Neuroscience and Neuropharmacology ResearchCell Adhesion Molecules ResearchGenetics and Neurodevelopmental Disorders

Activity-Dependent Regulation of Synaptic AMPA Receptor Composition and Abundance by β3 Integrins

Open access
Cingolani, Lorenzo A., Thalhammer, Agnes, Yu, Lily M.Y., Catalano, Myriam, Ramos, Timothy, Colicos, Michael A., Goda, Yukiko·2008·Neuron

Abstract

At synapses, cell adhesion molecules (CAMs) provide the molecular framework for coordinating signaling events across the synaptic cleft. Among synaptic CAMs, the integrins, receptors for extracellular matrix proteins and counterreceptors on adjacent cells, are implicated in synapse maturation and plasticity and memory formation. However, little is known about the molecular mechanisms of integrin action at central synapses. Here, we report that postsynaptic beta3 integrins control synaptic strength by regulating AMPA receptors (AMPARs) in a subunit-specific manner. Pharmacological perturbation targeting beta3 integrins promotes endocytosis of GluR2-containing AMPARs via Rap1 signaling, and expression of beta3 integrins produces robust changes in the abundance and composition of synaptic AMPARs without affecting dendritic spine structure. Importantly, homeostatic synaptic scaling induced by activity deprivation elevates surface expression of beta3 integrins, and in turn, beta3 integrins are required for synaptic scaling. Our findings demonstrate a key role for integrins in the feedback regulation of excitatory synaptic strength.

Integrity signals

Registry

Crossref · 10.1016/j.neuron.2008.04.011

Cites

69 of 69 references verified0 citation errors · 0 not checkable

Statistics

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

Claims the paper makes

We couldn’t retrieve this paper’s full text, 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?

  • The majority of studies that have blocked activity with TTX or AMPAR antagonists have observed a coordinated increase in GluA1 and GluA2.

    “the majority of studies that have blocked activity with tetrodotoxin (TTX) or AMPAR antagonists have observed a coordinated increase in GluA1 and GluA2 (O'Brien et al. 1998;Wierenga et al. 2005;Cingolani et al. 2008;Sun and Wolf 2009;Anggono et al. 2011; but see Thiagarajan et al. 2005).”
  • Interactions of ECM molecules with Narp complexes and integrins regulate AMPA and NMDA receptor subunit composition, synaptic clustering, and homeostatic synaptic scaling in GABAergic neurons.

    “Notable examples are interactions of ECM molecules with ‘neuronal activity-regulated pentraxin’ (Narp) complexes and integrins, shown to regulate AMPA and NMDA receptor subunit composition, synaptic clustering and homeostatic synaptic scaling in GABAergic neurons (Campo et al., 2009; Chang et al., 2010; Cingolani et al., 2008; Dityatev et al., 2010; Frischknecht and Gundelfinger, 2012).”

Cites

Flagged first, then by citations

1 of the 70 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Cingolani, L. A., Thalhammer, A., Yu, L. M. Y., Catalano, M., Ramos, T., Colicos, M. A., & Goda, Y.
Affiliations
  • MRC Laboratory for Molecular Cell Biology (GB)
  • University College London (GB)
  • University of Calgary (CA)
Corresponding author
  • Cingolani, Lorenzo A.
  • Goda, Yukiko
Venue
Neuron
Publisher
Elsevier BV
Published
2008-06
Volume
58
Issue
5
Pages
749-762
ISSN
0896-6273 (ISSN-L)
OpenAlex
W1983897183
Cited by
223
References
70
Citations by year
2026: 6 · 2025: 7 · 2024: 7 · 2023: 8 · 2022: 12 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 9 · 2017: 6 · 2016: 17 · 2015: 12 · 2014: 19 · 2013: 18 · 2012: 18
FWCI
8.50
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • ArTS Archivio della ricerca di Trieste (University of Trieste https://www.units.it/) (submittedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (R01MH066676, R01MH66676)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
CD61, AMPA receptors, GluR2, Rap1 signaling, synaptic scaling, homeostatic plasticity, activity-dependent regulation, synaptic efficacy, receptor internalization, dendritic spines, excitatory synapses
MeSH terms
Animals, Chelating Agents, Egtazic Acid, Endocytosis, Gene Expression Regulation, Hippocampus, Neural Inhibition, Neurons, Peptides, Platelet Aggregation Inhibitors, Synapses, Time Factors, Transfection, Presynaptic Terminals, Receptors, AMPA, Mice, Knockout, Patch-Clamp Techniques, Excitatory Amino Acids, Bridged Bicyclo Compounds, Heterocyclic, Excitatory Postsynaptic Potentials, rap1 GTP-Binding Proteins, Intercellular Signaling Peptides and Proteins, Integrin beta3, Mice, Rats, Thiazolidines, In Vitro Techniques

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