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dc.contributor.author
Vuillermot, Stéphanie
dc.contributor.author
Luan, Wei
dc.contributor.author
Meyer, Urs
dc.contributor.author
Eyles, Darryl
dc.date.accessioned
2019-10-04T14:21:26Z
dc.date.available
2017-06-12T20:25:25Z
dc.date.available
2019-10-04T14:21:26Z
dc.date.issued
2017
dc.identifier.issn
2040-2392
dc.identifier.other
10.1186/s13229-017-0125-0
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/129649
dc.identifier.doi
10.3929/ethz-b-000129649
dc.description.abstract
Background Prenatal exposure to infection is a recognized environmental risk factor for neuropsychiatric disorders of developmental origins such as autism or schizophrenia. Experimental work in animals indicates that this link is mediated by maternal immune activation (MIA) involving interactions between cytokine-associated inflammatory events, oxidative stress, and other pathophysiological processes such as hypoferremia and zinc deficiency. Maternal administration of the viral mimic polyriboinosinic-polyribocytidylic acid (poly(I:C)) in mice produces several behavioral phenotypes in adult offspring of relevance to autism spectrum disorder (ASD) and other neurodevelopmental disorders. Methods Here, we investigated whether some of these phenotypes might also present in juveniles. In addition, given the known immunomodulatory and neuroprotective effects of vitamin D, we also investigated whether the co-administration of vitamin D could block MIA-induced ASD-related behaviors. We co-administered the hormonally active form of vitamin D, 1α,25 dihydroxy vitamin D3 (1,25OHD), simultaneously with poly(I:C) and examined (i) social interaction, stereotyped behavior, emotional learning and memory, and innate anxiety-like behavior in juveniles and (ii) the levels of the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α in maternal plasma and fetal brains. Results We show that like adult offspring that were exposed to MIA, juveniles display similar deficits in social approach behavior. Juvenile MIA offspring also show abnormal stereotyped digging and impaired acquisition and expression of tone-cued fear conditioning. Importantly, our study reveals that prenatal administration of 1,25OHD abolishes all these behavioral deficits in poly(I:C)-treated juveniles. However, prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains suggesting the anti-inflammatory actions of vitamin D are not the critical mechanism for its preventive actions in this ASD animal model. Conclusions This work raises the possibility that early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
PubMed Central
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject
Maternal immune activation
en_US
dc.subject
Vitamin D
en_US
dc.subject
Neurodevelopmental disorders
en_US
dc.subject
Schizophrenia
en_US
dc.subject
Autism
en_US
dc.subject
Cytokines
en_US
dc.subject
Dopamine
en_US
dc.title
Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2017-03-07
ethz.journal.title
Molecular autism
ethz.journal.volume
8
en_US
ethz.journal.abbreviated
Mol. autism
ethz.pages.start
9
en_US
ethz.size
13 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.identifier.nebis
006123874
ethz.publication.status
published
en_US
ethz.date.deposited
2017-06-12T20:26:34Z
ethz.source
ECIT
ethz.identifier.importid
imp59365558e552a96960
ethz.ecitpid
pub:192633
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-15T03:30:03Z
ethz.rosetta.lastUpdated
2019-10-04T14:21:39Z
ethz.rosetta.versionExported
true
ethz.COinS
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