Evidence map›Paper›PMID 39423809›Full record

ArticleCell reports. Medicine2024

Neuropeptide therapeutics to repress lateral septum neurons that disable sociability in an autism mouse model.

Amélie M Borie, Yann Dromard, Prabahan Chakraborty, Pierre Fontanaud, Emilie M Andre, Amaury François, Pascal Colson, Françoise Muscatelli, Gilles Guillon, Michel G Desarménien and 1 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
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.

Amélie M BorieInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Yann DromardInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Prabahan ChakrabortyInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Pierre FontanaudInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Emilie M AndreInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France; Département de Maieutique, University of Montpellier, 34090 Montpellier, France.
Amaury FrançoisInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Pascal ColsonInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France; Department of Anesthesiology and Critical Care Medicine, Arnaud de Villeneuve Academic Hospital, Montpellier 34090 Montpellier, France.
Françoise MuscatelliInstitut de Neurobiologie de la Méditerranée, INSERM, University of Aix-Marseille, 13273 Marseille, France.
Gilles GuillonInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Michel G DesarménienInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France.
Freddy JeanneteauInstitut de Génomique Fonctionnelle, Department of Neuroscience, Stress Hormones and Plasticity Unit, University of Montpellier, INSERM, CNRS, 34090 Montpellier, France. Electronic address: freddy.jeanneteau@igf.cnrs.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Confronting oxytocin and vasopressin deficits in autism spectrum disorders and rare syndromes brought promises and disappointments for the treatment of social disabilities. We searched downstream of oxytocin and vasopressin for targets alleviating social deficits in a mouse model of Prader-Willi syndrome and Schaaf-Yang syndrome, both associated with high prevalence of autism. We found a population of neurons in the lateral septum-activated on termination of social contacts-which oxytocin and vasopressin inhibit as per degree of peer affiliation. These are somatostatin neurons expressing oxytocin receptors coupled to GABA-B signaling, which are inhibited via GABA-A channels by vasopressin-excited GABA neurons. Loss of oxytocin or vasopressin signaling recapitulated the disease phenotype. By contrast, deactivation of somatostatin neurons or receptor signaling alleviated social deficits of disease models by increasing the duration of contacts with mates and strangers. These findings provide new insights into the treatment framework of social disabilities in neuropsychiatric disorders.

Indexed as

Autistic DisorderDisease Models, AnimalNeuronsOxytocinSocial BehaviorAnimalsMaleMiceMice, Inbred C57BLNeuropeptidesReceptors, OxytocinSeptal NucleiSignal TransductionSomatostatinVasopressinsNeuropeptidesOxytocinReceptors, OxytocinSomatostatinVasopressinsautismMagel2optogeneticoxytocinPader-Williphotometrysocialsomatostatintreatmentvasopressin

Identifiers

PMID39423809
PMCPMC11604546

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.