Evidence map›Paper›PMID 24894704›Full record

ArticleNature communications2014

Synaptic recruitment of gephyrin regulates surface GABAA receptor dynamics for the expression of inhibitory LTP.

Enrica Maria Petrini, Tiziana Ravasenga, Torben J Hausrat, Giuliano Iurilli, Umberto Olcese, Victor Racine, Jean-Baptiste Sibarita, Tija C Jacob, Stephen J Moss, Fabio Benfenati and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

118 citing papers in PubMed, 195 citations in OpenAlex.

  1. ICER-Controlled inhibitory plasticity of amygdala engram neurons regulates fear memory precision.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  3. GABASynapse (New York, N.Y.) · 2026
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  6. Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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  9. Competition between glycine and GABAProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. AExperimental and therapeutic medicine · 2025
    Article
  11. Article
  12. Proteostasis regulation of GABABiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  20. Article

58 more citing papers are in PubMed but not listed here.

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

13 authors at 6 institutions in 5 countries.

Enrica Maria PetriniDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Tiziana RavasengaDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Torben J HausratCenter for Molecular Neurobiology (ZMNH), University Medical Center Hamburg Eppendorf, D-20251 Hamburg, Germany.
Giuliano IurilliDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Umberto OlceseDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Victor RacineInstitute of Molecular and Cell Biology, Proteos, Singapore 138673, Singapore.
Jean-Baptiste Sibarita1] Interdisciplinary Institute for Neuroscience, University of Bordeaux, F-33000 Bordeaux, France [2] CNRS UMR 5297, F-33000 Bordeaux, France.
Tija C JacobDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Stephen J MossDepartment of Neuroscience, Tufts University, 136 Harrison Avenue, Arnold 207 Boston, Massachusetts 0211, USA.
Fabio Benfenati1] Department of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy [2] Department of Experimental Medicine, University of Genova, 16163 Genova, Italy.
Paolo MediniDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Matthias KneusselCenter for Molecular Neurobiology (ZMNH), University Medical Center Hamburg Eppendorf, D-20251 Hamburg, Germany.
Andrea BarberisDepartment of Neuroscience and Brain Technologies, The Italian Institute of Technology, Via Morego 30, 16163 Genova, Italy.
Italian Institute of Technology · ITUniversity Medical Center Hamburg-Eppendorf · DEInstitute of Molecular and Cell Biology · SGInstitut Interdisciplinaire de Neuroscience · FRTufts University · USUniversity of Pittsburgh · US

Funding

Telethon GGP11043
6 · The paper itself

Abstract

Postsynaptic long-term potentiation of inhibition (iLTP) can rely on increased GABAA receptors (GABA(A)Rs) at synapses by promoted exocytosis. However, the molecular mechanisms that enhance the clustering of postsynaptic GABA(A)Rs during iLTP remain obscure. Here we demonstrate that during chemically induced iLTP (chem-iLTP), GABA(A)Rs are immobilized and confined at synapses, as revealed by single-particle tracking of individual GABA(A)Rs in cultured hippocampal neurons. Chem-iLTP expression requires synaptic recruitment of the scaffold protein gephyrin from extrasynaptic areas, which in turn is promoted by CaMKII-dependent phosphorylation of GABA(A)R-β3-Ser(383). Impairment of gephyrin assembly prevents chem-iLTP and, in parallel, blocks the accumulation and immobilization of GABA(A)Rs at synapses. Importantly, an increase of gephyrin and GABA(A)R similar to those observed during chem-iLTP in cultures were found in the rat visual cortex following an experience-dependent plasticity protocol that potentiates inhibitory transmission in vivo. Thus, phospho-GABA(A)R-β3-dependent accumulation of gephyrin at synapses and receptor immobilization are crucial for iLTP expression and are likely to modulate network excitability.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Carrier ProteinsCells, CulturedHippocampusLong-Term PotentiationMembrane ProteinsMiceNeural InhibitionNeuronsPhosphorylationRatsReceptors, GABA-AReceptors, N-Methyl-D-AspartateVisual CortexCalcium-Calmodulin-Dependent Protein Kinase Type 2Carrier ProteinsGabrb3 protein, mouseGabrb3 protein, ratgephyrinMembrane ProteinsReceptors, GABA-AReceptors, N-Methyl-D-Aspartate

Identifiers

PMID24894704
PMCPMC4059940
OpenAlexW2066144751

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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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.