Evidence map›Paper›PMID 27669960›Full record

ArticleNature communications2016

Molecular determinants for the strictly compartmentalized expression of kainate receptors in CA3 pyramidal cells.

Sabine Fièvre, Mario Carta, Ingrid Chamma, Virginie Labrousse, Olivier Thoumine, Christophe Mulle

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. The intracellular domain of the epilepsy protein PCDH19 regulates spine density in cortical neurons in vivo viaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Activation of Extrasynaptic Kainate Receptors Drives Hilar Mossy Cell Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Review
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  9. Article
  10. Article
  11. Article
  12. Review
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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

6 authors at 2 institutions in 1 country.

Sabine FièvreInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Mario CartaInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Ingrid ChammaInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Virginie LabrousseInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Olivier ThoumineInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Christophe MulleInterdisciplinary Institute for Neuroscience, CNRS UMR 5297, University of Bordeaux, 146 rue Léo-Saignat, F-33076 Bordeaux, France.
Institut Interdisciplinaire de Neuroscience · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Distinct subtypes of ionotropic glutamate receptors can segregate to specific synaptic inputs in a given neuron. Using functional mapping by focal glutamate uncaging in CA3 pyramidal cells (PCs), we observe that kainate receptors (KARs) are strictly confined to the postsynaptic elements of mossy fibre (mf) synapses and excluded from other glutamatergic inputs and from extrasynaptic compartments. By molecular replacement in organotypic slices from GluK2 knockout mice, we show that the faithful rescue of KAR segregation at mf-CA3 synapses critically depends on the amount of GluK2a cDNA transfected and on a sequence in the GluK2a C-terminal domain responsible for interaction with N-cadherin. Targeted deletion of N-cadherin in CA3 PCs greatly reduces KAR content in thorny excrescences and KAR-EPSCs at mf-CA3 synapses. Hence, multiple mechanisms combine to confine KARs at mf-CA3 synapses, including a stringent control of the amount of GluK2 subunit in CA3 PCs and the recruitment/stabilization of KARs by N-cadherins.

Identifiers

PMID27669960
PMCPMC5052629
OpenAlexW2527673213

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.