Cited by 565Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionGenetics and Neurodevelopmental Disorders

Unraveling mechanisms of homeostatic synaptic plasticity

Open access
Pozo, Karine, Goda, Yukiko·2010·Neuron

Abstract

Homeostatic synaptic plasticity is a negative feedback mechanism that neurons use to offset excessive excitation or inhibition by adjusting their synaptic strengths. Recent findings reveal a complex web of signaling processes involved in this compensatory form of synaptic strength regulation, and in contrast to the popular view of homeostatic plasticity as a slow, global phenomenon, neurons may also rapidly tune the efficacy of individual synapses on demand. Here we review our current understanding of cellular and molecular mechanisms of homeostatic synaptic plasticity.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.neuron.2010.04.028

Cites

176 of 176 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • Dendritic morphogenesis, synaptogenesis and continued activity-dependent remodelling of synaptic connections are critical for the development and maintenance of functional neuronal networks.

    “Dendritic morphogenesis, synaptogenesis and continued activity-dependent remodelling of synaptic connections are critical for the development and maintenance of functional neuronal networks.11, 12, 13, 14, 15”

    From The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines (2014) · cites this paper as [14]

    The Introduction describes activity-dependent changes in synaptic strength and their role in maintaining network stability. The Excitatory-inhibitory balance section also notes synapse remodeling in developing networks. Our copy does not establish the claimed importance of dendritic morphogenesis or synaptogenesis for developing and maintaining functional networks. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Kv7 channels furnish a non-inactivating M-current that stabilizes the axon initial segment; redistribution or pharmacologic enhancement reduces spurious spiking and limits burst afterdepolarizations.

    “Kv7 channels furnish a non-inactivating M-current that stabilizes the axon initial segment; redistribution or pharmacologic enhancement reduces spurious spiking and limits burst afterdepolarizations [360,362].”

    From Synaptic Plasticity—Intrinsic Excitability and Antidepressant Discovery (2026) · cites this paper as [360]

    The Excitatory-inhibitory balance section mentions developmental changes in the spatial distribution of ion channels and intrinsic excitability, but does not identify Kv7 channels. Searches for Kv7, M-current, the axon initial segment, and burst afterdepolarizations found no passage addressing the claimed mechanism or effects; page numbers were unavailable in our copy. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Pozo, K., & Goda, Y.
Affiliations
MRC Laboratory for Molecular Cell Biology (GB)
Corresponding author
Goda, Yukiko
Venue
Neuron
Publisher
Elsevier BV
Published
2010-05
Volume
66
Issue
3
Pages
337-351
ISSN
0896-6273 (ISSN-L)
OpenAlex
W2010356589
Cited by
565
References
176
Citations by year
2026: 20 · 2025: 41 · 2024: 19 · 2023: 29 · 2022: 29 · 2021: 33 · 2020: 37 · 2019: 31 · 2018: 36 · 2017: 31 · 2016: 31 · 2015: 40 · 2014: 34 · 2013: 47 · 2012: 54
FWCI
4.27
Type
journal article
Language
en
Open access
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
homeostatic plasticity, synaptic homeostasis, negative feedback, neuronal excitation, neuronal inhibition, synaptic efficacy, molecular mechanisms, cellular mechanisms
MeSH terms
Animals, Homeostasis, Models, Neurological, Nerve Net, Synaptic Transmission, Neuronal Plasticity, Neurons, Synapses

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