Evidence map›Paper›PMID 33615226›Full record

ArticleCerebral cortex communications2021

Behavioral Deficits in Mice with Postnatal Disruption of

Cezar Gavrilovici, Yulan Jiang, Ivana Kiroski, Toni-Lee Sterley, Milene Vandal, Jaideep Bains, Sang Ki Park, Jong M Rho, G Campbell Teskey, Minh Dang Nguyen

Open access · hybridAbstract read
In one paragraph

Article in Cerebral cortex communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 12 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

10 authors at 4 institutions in 3 countries.

Cezar GavriloviciDepartments of Neurosciences & Pediatrics, University of California San Diego, Rady Children's Hospital San Diego, San Diego, CA 92123, USA.
Yulan JiangDepartments of Clinical Neurosciences, Cell Biology and Anatomy, and Biochemistry and Molecular Biology, Hotchkiss Brain Institute, Calgary, AB T2N 4N1, Canada.
Ivana KiroskiDepartments of Clinical Neurosciences, Cell Biology and Anatomy, and Biochemistry and Molecular Biology, Hotchkiss Brain Institute, Calgary, AB T2N 4N1, Canada.
Toni-Lee SterleyDepartments of Physiology and Pharmacology, University of Calgary, Calgary, AB T2N 4N1, Canada.
Milene VandalDepartments of Clinical Neurosciences, Cell Biology and Anatomy, and Biochemistry and Molecular Biology, Hotchkiss Brain Institute, Calgary, AB T2N 4N1, Canada.
Jaideep BainsDepartments of Physiology and Pharmacology, University of Calgary, Calgary, AB T2N 4N1, Canada.
Sang Ki ParkDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 37673, Korea.
Jong M RhoDepartments of Neurosciences & Pediatrics, University of California San Diego, Rady Children's Hospital San Diego, San Diego, CA 92123, USA.
G Campbell TeskeyDepartment of Cell Biology and Anatomy, Hotchkiss Brain Institute, Calgary, AB T2N 4N1, Canada.
Minh Dang NguyenDepartments of Clinical Neurosciences, Cell Biology and Anatomy, and Biochemistry and Molecular Biology, Hotchkiss Brain Institute, Calgary, AB T2N 4N1, Canada.ORCID 0000-0003-4547-8617
University of Calgary · CAUniversity of California San Diego · USOntario Brain Institute · CAPohang University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunction of nuclear distribution element-like 1 (Ndel1) is associated with schizophrenia, a neuropsychiatric disorder characterized by cognitive impairment and with seizures as comorbidity. The levels of Ndel1 are also altered in human and models with epilepsy, a chronic condition whose hallmark feature is the occurrence of spontaneous recurrent seizures and is typically associated with comorbid conditions including learning and memory deficits, anxiety, and depression. In this study, we analyzed the behaviors of mice postnatally deficient for Ndel1 in forebrain excitatory neurons (Ndel1 CKO) that exhibit spatial learning and memory deficits, seizures, and shortened lifespan. Ndel1 CKO mice underperformed in species-specific tasks, that is, the nest building, open field, Y maze, forced swim, and dry cylinder tasks. We surveyed the expression and/or activity of a dozen molecules related to Ndel1 functions and found changes that may contribute to the abnormal behaviors. Finally, we tested the impact of Reelin glycoprotein that shows protective effects in the hippocampus of Ndel1 CKO, on the performance of the mutant animals in the nest building task. Our study highlights the importance of Ndel1 in the manifestation of species-specific animal behaviors that may be relevant to our understanding of the clinical conditions shared between neuropsychiatric disorders and epilepsy.

Indexed as

epilepsyhippocampusLis1 Reelinmouse behaviorNde1Ndel1schizophrenia

Identifiers

PMID33615226
PMCPMC7876307
OpenAlexW3119312125

What Socratic 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 Socratic graph.