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Article: Prenatal immune challenge is an environmental risk factor for brain and behavior change relevant to schizophrenia: Evidence from MRI in a mouse model
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TitlePrenatal immune challenge is an environmental risk factor for brain and behavior change relevant to schizophrenia: Evidence from MRI in a mouse model
 
AuthorsLi, Q2
Cheung, C2
Wei, R2
Hui, ES2
Feldon, J1
Meyer, U1
Chung, S2
Chua, SE2
Sham, PC2
Wu, EX2
McAlonan, GM2
 
Issue Date2009
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPlos One, 2009, v. 4 n. 7, article no. e6354 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0006354
 
AbstractObjectives: Maternal infection during pregnancy increases risk of severe neuropsychiatric disorders, including schizophrenia and autism, in the offspring. The most consistent brain structural abnormality in patients with schizophrenia is enlarged lateral ventricles. However, it is unknown whether the aetiology of ventriculomegaly in schizophrenia involves prenatal infectious processes. The present experiments tested the hypothesis that there is a causal relationship between prenatal immune challenge and emergence of ventricular abnormalities relevant to schizophrenia in adulthood. Method: We used an established mouse model of maternal immune activation (MIA) by the viral mimic Polyl:C administered in early (day 9) or late (day 17) gestation. Automated voxel-based morphometry mapped cerebrospinal fluid across the whole brain of adult offspring and the results were validated by manual region-of-interest tracing of the lateral ventricles. Parallel behavioral testing determined the existence of schizophrenia-related sensorimotor gating abnormalities. Results: Polyl:C-induced immune activation, in early but not late gestation, caused marked enlargement of lateral ventricles in adulthood, without affecting total white and grey matter volumes. This early exposure disrupted sensorimotor gating, in the form of prepulse inhibition. Identical immune challenge in late gestation resulted in significant expansion of 4th ventricle volume but did not disrupt sensorimotor gating. Conclusions: Our results provide the first experimental evidence that prenatal immune activation is an environmental risk factor for adult ventricular enlargement relevant to schizophrenia. The data indicate immune-associated environmental insults targeting early foetal development may have more extensive neurodevelopmental impact than identical insults in late prenatal life. © 2009 Li et al.
 
ISSN1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0006354
 
PubMed Central IDPMC2710518
 
ISI Accession Number IDWOS:000268318900006
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLi, Q
 
dc.contributor.authorCheung, C
 
dc.contributor.authorWei, R
 
dc.contributor.authorHui, ES
 
dc.contributor.authorFeldon, J
 
dc.contributor.authorMeyer, U
 
dc.contributor.authorChung, S
 
dc.contributor.authorChua, SE
 
dc.contributor.authorSham, PC
 
dc.contributor.authorWu, EX
 
dc.contributor.authorMcAlonan, GM
 
dc.date.accessioned2010-10-31T11:24:55Z
 
dc.date.available2010-10-31T11:24:55Z
 
dc.date.issued2009
 
dc.description.abstractObjectives: Maternal infection during pregnancy increases risk of severe neuropsychiatric disorders, including schizophrenia and autism, in the offspring. The most consistent brain structural abnormality in patients with schizophrenia is enlarged lateral ventricles. However, it is unknown whether the aetiology of ventriculomegaly in schizophrenia involves prenatal infectious processes. The present experiments tested the hypothesis that there is a causal relationship between prenatal immune challenge and emergence of ventricular abnormalities relevant to schizophrenia in adulthood. Method: We used an established mouse model of maternal immune activation (MIA) by the viral mimic Polyl:C administered in early (day 9) or late (day 17) gestation. Automated voxel-based morphometry mapped cerebrospinal fluid across the whole brain of adult offspring and the results were validated by manual region-of-interest tracing of the lateral ventricles. Parallel behavioral testing determined the existence of schizophrenia-related sensorimotor gating abnormalities. Results: Polyl:C-induced immune activation, in early but not late gestation, caused marked enlargement of lateral ventricles in adulthood, without affecting total white and grey matter volumes. This early exposure disrupted sensorimotor gating, in the form of prepulse inhibition. Identical immune challenge in late gestation resulted in significant expansion of 4th ventricle volume but did not disrupt sensorimotor gating. Conclusions: Our results provide the first experimental evidence that prenatal immune activation is an environmental risk factor for adult ventricular enlargement relevant to schizophrenia. The data indicate immune-associated environmental insults targeting early foetal development may have more extensive neurodevelopmental impact than identical insults in late prenatal life. © 2009 Li et al.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationPlos One, 2009, v. 4 n. 7, article no. e6354 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0006354
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0006354
 
dc.identifier.eissn1932-6203
 
dc.identifier.epagearticle no. e6354
 
dc.identifier.hkuros174144
 
dc.identifier.isiWOS:000268318900006
 
dc.identifier.issn1932-6203
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
 
dc.identifier.issue7
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC2710518
 
dc.identifier.pmid19629183
 
dc.identifier.scopuseid_2-s2.0-67749147581
 
dc.identifier.spagee6354
 
dc.identifier.spagearticle no. e6354
 
dc.identifier.urihttp://hdl.handle.net/10722/125328
 
dc.identifier.volume4
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshBehavior, Animal
 
dc.subject.meshBrain - pathology
 
dc.subject.meshDisease Models, Animal
 
dc.subject.meshMagnetic Resonance Imaging - methods
 
dc.subject.meshMaternal Exposure
 
dc.titlePrenatal immune challenge is an environmental risk factor for brain and behavior change relevant to schizophrenia: Evidence from MRI in a mouse model
 
dc.typeArticle
 
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<contributor.author>Feldon, J</contributor.author>
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<contributor.author>Chua, SE</contributor.author>
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Author Affiliations
  1. Eidgenossische Technische Hochschule Zurich
  2. The University of Hong Kong