Evidence map›Paper›PMID 26946128›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

Cortical Structure Alterations and Social Behavior Impairment in p50-Deficient Mice.

Sara Anna Bonini, Andrea Mastinu, Giuseppina Maccarinelli, Stefania Mitola, Marika Premoli, Luca Rosario La Rosa, Giulia Ferrari-Toninelli, Mariagrazia Grilli, Maurizio Memo

Open access · hybridAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 37 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

9 authors at 2 institutions in 1 country.

Sara Anna BoniniDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Andrea MastinuDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Giuseppina MaccarinelliDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Stefania MitolaDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Marika PremoliDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Luca Rosario La RosaDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Giulia Ferrari-ToninelliDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
Mariagrazia GrilliLaboratory of Neuroplasticity, Department of Pharmaceutical Sciences, University of Piemonte Orientale, 28100 Novara, Italy.
Maurizio MemoDepartment of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy.
University of Brescia · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alterations in genes that regulate neurodevelopment can lead to cortical malformations, resulting in malfunction during postnatal life. The NF-κB pathway has a key role during neurodevelopment by regulating the maintenance of the neural progenitor cell pool and inhibiting neuronal differentiation. In this study, we evaluated whether mice lacking the NF-κB p50 subunit (KO) present alterations in cortical structure and associated behavioral impairment. We found that, compared with wild type (WT), KO mice at postnatal day 2 present an increase in radial glial cells, an increase in Reelin protein expression levels, in addition to an increase of specific layer thickness. Moreover, adult KO mice display abnormal columnar organization in the somatosensory cortex, a specific decrease in somatostatin- and parvalbumin-expressing interneurons, altered neurite orientation, and a decrease in Synapsin I protein levels. Concerning behavior, KO mice, in addition to an increase in locomotor and exploratory activity, display impairment in social behaviors, with a reduction in social interaction. Finally, we found that risperidone treatment decreased hyperactivity of KO mice, but had no effect on defective social interaction. Altogether, these data add complexity to a growing body of data, suggesting a link between dysregulation of the NF-κB pathway and neurodevelopmental disorders pathogenesis.

Indexed as

Social BehaviorAnimalsBrainCell Adhesion Molecules, NeuronalEpendymoglial CellsExploratory BehaviorExtracellular Matrix ProteinsInterneuronsMaleMice, KnockoutMotor ActivityNerve Tissue ProteinsNeuritesNF-kappa B p50 SubunitParvalbuminsReelin ProteinCell Adhesion Molecules, NeuronalExtracellular Matrix ProteinsNerve Tissue ProteinsNF-kappa B p50 SubunitParvalbuminsReelin ProteinReln protein, mouseRisperidoneSerine EndopeptidasesSomatostatinSynapsinsTranquilizing Agentscortical structureneurodevelopmental disordersNF-κBp50−/− micesocial behavior

Identifiers

PMID26946128
PMCPMC4869818
OpenAlexW2295421533

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.