Evidence map›Paper›PMID 33666173›Full record

ArticleeLife2021

Sequential perturbations to mouse corticogenesis following in utero maternal immune activation.

Cesar P Canales, Myka L Estes, Karol Cichewicz, Kartik Angara, John Paul Aboubechara, Scott Cameron, Kathryn Prendergast, Linda Su-Feher, Iva Zdilar, Ellie J Kreun and 11 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Genes · 2026
    Article
  2. Article
  3. Mild SARS-CoV-2 maternal infection in mice induces transient offspring neurodevelopmental aberrance.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Differential effects of early or late exposure to prenatal maternal immune activation on mouse embryonic neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  20. Krüppel-like Transcription Factor 7 Is a Causal Gene in Autism Development.International journal of molecular sciences · 2022
    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

21 authors at 3 institutions in 1 country.

Cesar P Canales *Center for Neuroscience, UC Davis, Davis, United States.ORCID 0000-0003-2505-8367
Myka L Estes *Center for Neuroscience, UC Davis, Davis, United States.
Karol Cichewicz *Center for Neuroscience, UC Davis, Davis, United States.ORCID 0000-0001-5926-3663
Kartik AngaraDepartment of Pediatrics & Human Development, Michigan State University, East Lansing, United States.
John Paul AboubecharaCenter for Neuroscience, UC Davis, Davis, United States.
Scott CameronCenter for Neuroscience, UC Davis, Davis, United States.
Kathryn PrendergastCenter for Neuroscience, UC Davis, Davis, United States.
Linda Su-FeherCenter for Neuroscience, UC Davis, Davis, United States.
Iva ZdilarCenter for Neuroscience, UC Davis, Davis, United States.
Ellie J KreunCenter for Neuroscience, UC Davis, Davis, United States.
Emma C ConnollyCenter for Neuroscience, UC Davis, Davis, United States.
Jin Myeong SeoCenter for Neuroscience, UC Davis, Davis, United States.
Jack B GoonCenter for Neuroscience, UC Davis, Davis, United States.
Kathleen FarrellyCenter for Neuroscience, UC Davis, Davis, United States.
Tyler W StradleighCenter for Neuroscience, UC Davis, Davis, United States.
Deborah van der ListCenter for Neuroscience, UC Davis, Davis, United States.
Lori HaapanenDivision of Rheumatology, Allergy and Clinical Immunology, UC Davis, Davis, United States.
Judy Van de WaterDivision of Rheumatology, Allergy and Clinical Immunology, UC Davis, Davis, United States.
Daniel VogtDepartment of Pediatrics & Human Development, Michigan State University, East Lansing, United States.
A Kimberley McAllister *Center for Neuroscience, UC Davis, Davis, United States.ORCID 0000-0001-9177-9889
Alex S Nord *Center for Neuroscience, UC Davis, Davis, United States.ORCID 0000-0003-4259-7514
Center for Neurosciences · USMichigan State University · USUniversity of California, Davis · US

Funding

UC Davis Conte Center: Neuroimmune Mechanisms of Psychiatric DisordersP50MH106438 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARTER, CAMERON S. · 2015 to 2025
$26.1M
Interdisciplinary Training for Autism Researchers(RMI)T32MH073124 · NIMH · UNIVERSITY OF CALIFORNIA DAVIS · PI Stephen Charles Noctor, Christine Wu Nordahl · 2004 to 2026
$6.8M
Functional Elucidation of the Sequence-Encoded Regulatory Activity of Enhancers in Vivo in the BrainR35GM119831 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Alexander Nord · 2016 to 2026
$3.9M
Learning, Memory, and Plasticity (LaMP) Training ProgramT32MH112507 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Karen Zito · 2017 to 2026
$2.4M
Prenatal brain development following maternal immune activationR21MH116681 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MCALLISTER, A KIMBERLEY, NORD, ALEXANDER · 2018 to 2019
$432k
NIGMS NIH HHS GM119831NIGMS NIH HHS R35 GM119831NIMH NIH HHS 2T32MH073124-16NIMH NIH HHS P50 MH106438NIMH NIH HHS R21 MH116681NIMH NIH HHS T32 MH073124NIMH NIH HHS T32 MH112507
6 · The paper itself

Abstract

In utero exposure to maternal immune activation (MIA) is an environmental risk factor for neurodevelopmental and neuropsychiatric disorders. Animal models provide an opportunity to identify mechanisms driving neuropathology associated with MIA. We performed time-course transcriptional profiling of mouse cortical development following induced MIA via poly(I:C) injection at E12.5. MIA-driven transcriptional changes were validated via protein analysis, and parallel perturbations to cortical neuroanatomy were identified via imaging. MIA-induced acute upregulation of genes associated with hypoxia, immune signaling, and angiogenesis, by 6 hr following exposure. This acute response was followed by changes in proliferation, neuronal and glial specification, and cortical lamination that emerged at E14.5 and peaked at E17.5. Decreased numbers of proliferative cells in germinal zones and alterations in neuronal and glial populations were identified in the MIA-exposed cortex. Overall, paired transcriptomic and neuroanatomical characterization revealed a sequence of perturbations to corticogenesis driven by mid-gestational MIA.

Indexed as

NeurogenesisAnimalsBrainDisease Models, AnimalFemaleMaleMiceMice, Inbred C57BLNeurodevelopmental DisordersPoly I-CPregnancyPrenatal Exposure Delayed EffectsTranscriptomePoly I-Cbrain developmentgeneticsgenomicsMIAmouseneuroscienceRNA-SeqtranscriptomicWGCNA

Identifiers

PMID33666173
PMCPMC7979158
OpenAlexW3135675186

What OpenQuestion holds

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Registered trials

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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.