Evidence map›Paper›PMID 23864664›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Persistent synaptic scaling independent of AMPA receptor subunit composition.

Haider F Altimimi, David Stellwagen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Diverging from the Norm: Reevaluating What Miniature Excitatory Postsynaptic Currents Tell Us about Homeostatic Synaptic Plasticity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  5. Article
  6. Divergent Synaptic Scaling of Miniature EPSCs following Activity Blockade in Dissociated Neuronal Cultures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  7. Article
  8. TNF-Mediated Homeostatic Synaptic Plasticity: FromFrontiers in cellular neuroscience · 2020
    Review
  9. Review
  10. Review
  11. Article
  12. Control of Homeostatic Synaptic Plasticity by AKAP-Anchored Kinase and Phosphatase Regulation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  13. Review
  14. Synaptic homeostasis requires the membrane-proximal carboxy tail of GluA2.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  15. Article
  16. Article
  17. Activity-dependent synaptic GRIP1 accumulation drives synaptic scaling up in response to action potential blockade.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. The role of GluA1 in ocular dominance plasticity in the mouse visual cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Haider F AltimimiCentre for Research in Neuroscience, Department of Neurology and Neurosurgery, The Research Institute of the McGill University Health Centre, Montreal, Quebec H3G 1A4, Canada.
David Stellwagen
McGill University Health Centre · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Despite long-standing evidence that the specific intracellular domains of AMPA-type glutamate receptor (AMPAR) subunits are critical for trafficking, it has recently been demonstrated that there is no absolute requirement for any AMPAR subunit for the receptor insertion underlying LTP. It is unclear whether this holds true to other forms of plasticity. Homeostatic synaptic plasticity (HSP) is an important form of negative feedback that provides stability to neuronal networks, and results at least in part from the insertion of AMPARs into glutamatergic synapses following chronic reductions in neuronal activity. Similar to LTP, the GluA1 subunit has been suggested to be the requisite subunit for HSP-induced AMPAR insertion and acute treatment with signaling molecules that underlie some forms of HSP results in the preferential incorporation of GluA2-lacking receptors. However, knockdown experiments have instead implicated a requirement for the GluA2 subunit. Here we re-examined the requirement for specific AMPAR subunit during chronic tetrodotoxin-induced HSP using hippocampal cultures derived from AMPAR subunit knock-out mice. We observed HSP in cultures from GluA1⁻/⁻, GluA2⁻/⁻, and GluA2⁻/⁻ GluA3⁻/⁻ mice, and conclude that, as with LTP, there is no subunit requirement for HSP.

Indexed as

AnimalsCells, CulturedExcitatory Postsynaptic PotentialsHippocampusMiceMice, KnockoutMiniature Postsynaptic PotentialsNerve NetNeuronal PlasticityProtein SubunitsReceptors, AMPASynapsesSynaptic TransmissionProtein SubunitsReceptors, AMPA

Identifiers

PMID23864664
PMCPMC6794055
OpenAlexW2018253174

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.