Evidence map›Paper›PMID 32919409›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2021

Transgenerational modification of dopaminergic dysfunctions induced by maternal immune activation.

Ulrike Weber-Stadlbauer, Juliet Richetto, Ramona A J Zwamborn, Roderick C Slieker, Urs Meyer

Open access · hybridAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

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  18. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
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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

5 authors at 3 institutions in 2 countries.

Ulrike Weber-StadlbauerInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland. ulrike.weber@uzh.ch.ORCID http://orcid.org/0000-0002-5278-9993
Juliet RichettoInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.
Ramona A J ZwambornDepartment of Neurology, UMC Utrecht Brain Center, Utrecht, The Netherlands.
Roderick C SliekerDepartment of Biomedical Data Sciences, Section Molecular Epidemiology, Leiden, The Netherlands.ORCID http://orcid.org/0000-0003-0961-9152
Urs MeyerInstitute of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland.ORCID http://orcid.org/0000-0001-7244-0345
University of Zurich · CHLeiden University Medical Center · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prenatal exposure to infectious and/or inflammatory insults is increasingly recognized to contribute to the etiology of psychiatric disorders with neurodevelopmental components. Recent research using animal models suggests that maternal immune activation (MIA) can induce transgenerational effects on brain and behavior, possibly through epigenetic mechanisms. Using a mouse model of MIA that is based on gestational treatment with the viral mimeticpoly(I:C) (= polyriboinosinic-polyribocytidilic acid), the present study explored whether the transgenerational effects of MIA are extendable to dopaminergic dysfunctions. We show that the direct descendants born to poly(I:C)-treated mothers display signs of hyperdopaminergia, as manifested by a potentiated sensitivity to the locomotor-stimulating effects of amphetamine (Amph) and increased expression of tyrosine hydroxylase (Th) in the adult ventral midbrain. In stark contrast, second- and third-generation offspring of MIA-exposed ancestors displayed blunted locomotor responses to Amph and reduced expression of Th. Furthermore, we found increased DNA methylation at the promoter region of the dopamine-specifying factor, nuclear receptor-related 1 protein (Nurr1), in the sperm of first-generation MIA offspring and in the ventral midbrain of second-generation offspring of MIA-exposed ancestors. The latter effect was further accompanied by reduced mRNA levels of Nurr1 in this brain region. Together, our results suggest that MIA has the potential to modify dopaminergic functions across multiple generations with opposite effects in the direct descendants and their progeny. The presence of altered DNA methylation in the sperm of MIA-exposed offspring highlights the possibility that epigenetic processes in the male germline play a role in the transgenerational effects of MIA.

Indexed as

Behavior, AnimalPrenatal Exposure Delayed EffectsAnimalsDisease Models, AnimalDopamineFemalePoly I-CPregnancyDopaminePoly I-C

Identifiers

PMID32919409
PMCPMC7852665
OpenAlexW3086828095

What OpenQuestion holds

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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.