Evidence map›Paper›PMID 34815409›Full record

ArticleNature communications2021

Developmental decrease of entorhinal-hippocampal communication in immune-challenged DISC1 knockdown mice.

Xiaxia Xu, Lingzhen Song, Rebecca Kringel, Ileana L Hanganu-Opatz

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Olfactory processing in gifted and non-gifted children: assessing the sniffin' sticks olfactory test for threshold, discrimination, and identification abilities.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  4. Developmental Olfactory Dysfunction and Abnormal Odor Memory in Immune-ChallengedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
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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

4 authors at 1 institution in 1 country.

Xiaxia XuInstitute of Developmental Neurophysiology, Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. xiaxia.xu@zmnh.uni-hamburg.de.ORCID http://orcid.org/0000-0001-8106-8901
Lingzhen SongInstitute of Developmental Neurophysiology, Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany.
Rebecca KringelInstitute of Developmental Neurophysiology, Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany.
Ileana L Hanganu-OpatzInstitute of Developmental Neurophysiology, Center for Molecular Neurobiology, University Medical Center Hamburg-Eppendorf, 20251, Hamburg, Germany. hangop@zmnh.uni-hamburg.de.ORCID http://orcid.org/0000-0002-4787-1765
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prefrontal-hippocampal dysfunction that underlies cognitive deficits in mental disorders emerges during early development. The lateral entorhinal cortex (LEC) is tightly interconnected with both prefrontal cortex (PFC) and hippocampus (HP), yet its contribution to the early dysfunction is fully unknown. Here we show that mice that mimic the dual genetic (G) -environmental (E) etiology (GE mice) of psychiatric risk have poor LEC-dependent recognition memory at pre-juvenile age and abnormal communication within LEC-HP-PFC networks throughout development. These functional and behavioral deficits relate to sparser projections from LEC to CA1 and decreased efficiency of axonal terminals to activate the hippocampal circuits in neonatal GE mice. In contrast, the direct entorhinal drive to PFC is not affected, yet the PFC is indirectly compromised, as target of the under-activated HP. Thus, the entorhinal-hippocampal circuit is already impaired from neonatal age on in GE mice.

Indexed as

AnimalsAnimals, NewbornCA1 Region, HippocampalCognitive DysfunctionDisease Models, AnimalEntorhinal CortexFemaleGene-Environment InteractionHumansMaleMental DisordersMiceMice, TransgenicNerve Tissue ProteinsNeural PathwaysOptogeneticsDisc1 protein, mouseNerve Tissue Proteins

Identifiers

PMID34815409
PMCPMC8611076
OpenAlexW3215508974

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.