Evidence map›Paper›PMID 31891351›Full record

ArticleeLife2019

Activity-dependent death of transient Cajal-Retzius neurons is required for functional cortical wiring.

Martina Riva, Ioana Genescu, Chloé Habermacher, David Orduz, Fanny Ledonne, Filippo M Rijli, Guillermina López-Bendito, Eva Coppola, Sonia Garel, Maria Cecilia Angulo and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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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

11 authors at 4 institutions in 3 countries.

Martina Riva *Institut Imagine, Université de Paris, Paris, France.
Ioana Genescu *Institut de Biologie de l'École Normale Supérieure (IBENS), Département de Biologie, École Normale Supérieure, CNRS, INSERM, Université PSL, Paris, France.
Chloé Habermacher *Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Université de Paris, Paris, France.
David OrduzINSERM U1128, Paris, France.ORCID 0000-0002-4198-2691
Fanny LedonneInstitut Jacques Monod, CNRS UMR 7592, Université de Paris, Paris, France.
Filippo M RijliFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.ORCID 0000-0003-0515-0182
Guillermina López-BenditoInstituto de Neurosciencias de Alicante, Universidad Miguel Hernandez, Sant Joan d'Alacant, Spain.
Eva CoppolaInstitut Imagine, Université de Paris, Paris, France.
Sonia Garel *Institut de Biologie de l'École Normale Supérieure (IBENS), Département de Biologie, École Normale Supérieure, CNRS, INSERM, Université PSL, Paris, France.ORCID 0000-0003-2984-3645
Maria Cecilia Angulo *Institute of Psychiatry and Neuroscience of Paris (IPNP), INSERM U1266, Université de Paris, Paris, France.ORCID 0000-0002-0758-0496
Alessandra Pierani *Institut Imagine, Université de Paris, Paris, France.ORCID 0000-0002-4872-4791
Centre National de la Recherche Scientifique · FRInserm · FRColumbia University · USFriedrich Miescher Institute · CH

Funding

Agence Nationale de la Recherche ANR-15-CE16-0003-01European Commission ERC-2013-CoG-616080European Commission ERC-2014-CoG-647012Fondation pour l'Aide à la Recherche sur la Sclérose en Plaques Postdoctoral fellowshipFondation pour la Recherche Médicale Equipe (DEQ20130326521)Fondation pour la Recherche Médicale Equipe (DEQ20150331681)Ministry of Higher Education, Research and Innovation FellowshipMinistry of Science, Innovation and Universities BFU2015-64432-R
6 · The paper itself

Abstract

Programmed cell death and early activity contribute to the emergence of functional cortical circuits. While most neuronal populations are scaled-down by death, some subpopulations are entirely eliminated, raising the question of the importance of such demise for cortical wiring. Here, we addressed this issue by focusing on Cajal-Retzius neurons (CRs), key players in cortical development that are eliminated in postnatal mice in part via Bax-dependent apoptosis. Using Bax-conditional mutants and CR hyperpolarization, we show that the survival of electrically active subsets of CRs triggers an increase in both dendrite complexity and spine density of upper layer pyramidal neurons, leading to an excitation/inhibition imbalance. The survival of these CRs is induced by hyperpolarization, highlighting an interplay between early activity and neuronal elimination. Taken together, our study reveals a novel activity-dependent programmed cell death process required for the removal of transient immature neurons and the proper wiring of functional cortical circuits.

Indexed as

AnimalsAnimals, NewbornApoptosisbcl-2-Associated X ProteinCell PolarityCerebral CortexElectric StimulationInterstitial Cells of CajalMiceMutant ProteinsNeurogenesisPyramidal CellsBax protein, mousebcl-2-Associated X ProteinMutant ProteinsapoptosisCajal-Retzius neuronscortical developmentdevelopmental biologyexcitation/inhibition ratiomouseneuronal activityneurosciencetransient

Identifiers

PMID31891351
PMCPMC6938399
OpenAlexW2997583973

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.