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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

TitlePrenatal immune challenge is an environmental risk factor for brain and behavior change relevant to schizophrenia: Evidence from MRI in a mouse model
Authors
Issue Date2009
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2009, v. 4 n. 7, article no. e6354 How to Cite?
Abstract
Objectives: 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.
Persistent Identifierhttp://hdl.handle.net/10722/125328
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, Qen_HK
dc.contributor.authorCheung, Cen_HK
dc.contributor.authorWei, Ren_HK
dc.contributor.authorHui, ESen_HK
dc.contributor.authorFeldon, Jen_HK
dc.contributor.authorMeyer, Uen_HK
dc.contributor.authorChung, Sen_HK
dc.contributor.authorChua, SEen_HK
dc.contributor.authorSham, PCen_HK
dc.contributor.authorWu, EXen_HK
dc.contributor.authorMcAlonan, GMen_HK
dc.date.accessioned2010-10-31T11:24:55Z-
dc.date.available2010-10-31T11:24:55Z-
dc.date.issued2009en_HK
dc.identifier.citationPlos One, 2009, v. 4 n. 7, article no. e6354en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125328-
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.en_HK
dc.languageengen_HK
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
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 modelen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=4&issue=7&spage=e6354&epage=&date=2009&atitle=Prenatal+immune+challenge+is+an+environmental+risk+factor+for+brain+and+behavior+change+relevant+to+schizophrenia:+evidence+from+MRI+in+a+mouse+model-
dc.identifier.emailCheung, C: charlton@hkucc.hku.hken_HK
dc.identifier.emailChung, S: skchung@hkucc.hku.hken_HK
dc.identifier.emailChua, SE: sechua@hku.hken_HK
dc.identifier.emailSham, PC: pcsham@hku.hken_HK
dc.identifier.emailWu, EX: ewu1@hkucc.hku.hken_HK
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hken_HK
dc.identifier.authorityCheung, C=rp01574en_HK
dc.identifier.authorityChung, S=rp00381en_HK
dc.identifier.authorityChua, SE=rp00438en_HK
dc.identifier.authoritySham, PC=rp00459en_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.identifier.authorityMcAlonan, GM=rp00475en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0006354en_HK
dc.identifier.pmid19629183-
dc.identifier.pmcidPMC2710518-
dc.identifier.scopuseid_2-s2.0-67749147581en_HK
dc.identifier.hkuros174144en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67749147581&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume4en_HK
dc.identifier.issue7en_HK
dc.identifier.spagee6354en_HK
dc.identifier.spagearticle no. e6354-
dc.identifier.epagearticle no. e6354-
dc.identifier.eissn1932-6203-
dc.identifier.isiWOS:000268318900006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, Q=22034705700en_HK
dc.identifier.scopusauthoridCheung, C=7202061845en_HK
dc.identifier.scopusauthoridWei, R=34769199800en_HK
dc.identifier.scopusauthoridHui, ES=16175117100en_HK
dc.identifier.scopusauthoridFeldon, J=7102146902en_HK
dc.identifier.scopusauthoridMeyer, U=35196427300en_HK
dc.identifier.scopusauthoridChung, S=7404292976en_HK
dc.identifier.scopusauthoridChua, SE=7201550427en_HK
dc.identifier.scopusauthoridSham, PC=34573429300en_HK
dc.identifier.scopusauthoridWu, EX=7202128034en_HK
dc.identifier.scopusauthoridMcAlonan, GM=6603123011en_HK

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