Evidence map›Paper›PMID 36982451›Full record

ArticleInternational journal of molecular sciences2023

Activation of the PI3K/AKT/mTOR Pathway in Cajal-Retzius Cells Leads to Their Survival and Increases Susceptibility to Kainate-Induced Seizures.

Nasim Ramezanidoraki, Driss El Ouardi, Margaux Le, Stéphanie Moriceau, Mahboubeh Ahmadi, Dossi Elena, Danae Rolland, Philippe Bun, Gwenaëlle Le Pen, Guillaume Canaud and 5 more

Open access · goldFull text read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Partial Deletion ofeNeuro · 2026
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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

15 authors at 2 institutions in 1 country.

Nasim RamezanidorakiInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Driss El OuardiInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Margaux LeInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Stéphanie MoriceauPlatform for Neurobehavioral and Metabolism, Structure Fédérative de Recherche Necker, 26 INSERM US24/CNRS UAR 3633, 75015 Paris, France.ORCID 0000-0002-1413-9359
Mahboubeh AhmadiInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Dossi ElenaCenter for Interdisciplinary Research in Biology (CIRB), College de France, Centre National de Recherche Scientifique (CNRS), INSERM, Labex Memolife, Université Paris Sciences & Lettres (PSL), 75005 Paris, France.
Danae RollandInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Philippe BunInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.ORCID 0000-0002-7975-1768
Gwenaëlle Le PenInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Guillaume CanaudInstitut Necker Enfants-Malades (INEM), INSERM U1151, Université Paris Cité, 75015 Paris, France.
Nadia Bahi-BuissonInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Nathalie RouachCenter for Interdisciplinary Research in Biology (CIRB), College de France, Centre National de Recherche Scientifique (CNRS), INSERM, Labex Memolife, Université Paris Sciences & Lettres (PSL), 75005 Paris, France.ORCID 0000-0002-5574-888X
Rebecca PiskorowskiInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.ORCID 0000-0003-0120-2360
Alessandra PieraniInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.
Pierre BilluartInstitute of Psychiatry and Neuroscience of Paris (IPNP), Institut National de la Santé et de la Recherche Médicale (INSERM) U1266, Université Paris Cité (UPC), 75014 Paris, France.ORCID 0000-0003-1913-1687
Inserm · FRCentre National de la Recherche Scientifique · FR

Funding

Agence Nationale de la Recherche ANR-18-RHUS-005 ,ANR-10-IAHU-01,ANR-15-CE16-0003-01,ANR-20- CE16-0001-01, ANR-19-CE16-0017-03CNRS to A.P.Fondation pour la Recherche Médicale FRM DEQ20130326521 , EQU201903007836INSERM to P.B.The Network of European Funding for Neuroscience Research Era-Net Neuron ROSSINI
6 · The paper itself

Abstract

Cajal-Retzius cells (CRs) are a class of transient neurons in the mammalian cortex that play a critical role in cortical development. Neocortical CRs undergo almost complete elimination in the first two postnatal weeks in rodents and the persistence of CRs during postnatal life has been detected in pathological conditions related to epilepsy. However, it is unclear whether their persistence is a cause or consequence of these diseases. To decipher the molecular mechanisms involved in CR death, we investigated the contribution of the PI3K/AKT/mTOR pathway as it plays a critical role in cell survival. We first showed that this pathway is less active in CRs after birth before massive cell death. We also explored the spatio-temporal activation of both AKT and mTOR pathways and reveal area-specific differences along both the rostro-caudal and medio-lateral axes. Next, using genetic approaches to maintain an active pathway in CRs, we found that the removal of either PTEN or TSC1, two negative regulators of the pathway, lead to differential CR survivals, with a stronger effect in the

Indexed as

Kainic AcidProto-Oncogene Proteins c-aktAnimalsFemaleMammalsPhosphatidylinositol 3-KinasesSeizuresTOR Serine-Threonine KinasesKainic AcidPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCajal–Retzius cellsdevelopmentneuronal survivalPI3K/AKT/mTOR pathway

Identifiers

PMID36982451
PMCPMC10048971
OpenAlexW4324096909

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read75
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.