Evidence map›Paper›PMID 26247861›Full record

ArticleNeuron2015

Synaptic Consolidation Normalizes AMPAR Quantal Size following MAGUK Loss.

Jonathan M Levy, Xiaobing Chen, Thomas S Reese, Roger A Nicoll

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  10. Distinct SAP102 and PSD-95 Nano-organization Defines Multiple Types of Synaptic Scaffold Protein Domains at Single Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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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

4 authors at 3 institutions in 1 country.

Jonathan M LevyNeuroscience Graduate Program, University of California San Francisco, San Francisco, CA 94158, USA; Department of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA 94158, USA.
Xiaobing ChenLaboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Thomas S ReeseLaboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Roger A NicollDepartment of Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, CA 94158, USA. Electronic address: roger.nicoll@ucsf.edu.
University of California, San Francisco · USNational Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Macromolecular Architecture Of The SynapseZIANS002972 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI REESE, THOMAS S · 2009 to 2025
$25.6M
NEUROTRANSMITTER EFFECTS ON LOCAL NEURONAL CIRCUITSR37MH038256 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 1987 to 2016
$9.0M
Synaptic Plasticity Regulated by Stargazin-like gamma-8R01MH070957 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 2004 to 2019
$6.3M
Synaptic Glutamate Receptor Trafficking.R01MH080379 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NICOLL, ROGER A · 2007 to 2016
$5.3M
NIMH NIH HHS R01 MH070957NIMH NIH HHS R01 MH080379NIMH NIH HHS R37 MH038256
6 · The paper itself

Abstract

The mechanisms controlling synapse growth and maintenance are of critical importance for learning and memory. The MAGUK family of synaptic scaffolding proteins is abundantly expressed at glutamatergic central synapses, but their importance in controlling the synaptic content of glutamate receptors is poorly understood. Here, we use a chained RNAi-mediated knockdown approach to simultaneously remove PSD-93, PSD-95, and SAP102, the MAGUKs previously shown to be responsible for synaptic localization of glutamate receptors. We find that MAGUKs are specifically responsible for creating functional synapses after initial spine formation by filling functionally silent spines with glutamate receptors. Removal of the MAGUKs causes a transient reduction in AMPA receptor quantal size followed by synaptic consolidation resulting in a normalization of quantal size at the few remaining functional synapses. Consolidation requires signaling through L-type calcium channels, CaM kinase kinase, and the GluA2 AMPA receptor subunit, akin to a homeostatic process.

Indexed as

AnimalsDisks Large Homolog 4 ProteinHippocampusHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsNeuropeptidesOrgan Culture TechniquesRatsReceptors, AMPASynapsesSynaptic TransmissionDisks Large Homolog 4 ProteinDlg3 protein, ratDlg4 protein, ratIntracellular Signaling Peptides and ProteinsMembrane ProteinsMpp2 protein, ratNeuropeptidesReceptors, AMPA

Identifiers

PMID26247861
PMCPMC4596923
OpenAlexW1657343628

What OpenQuestion holds

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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.