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Conference Paper: Evidence that prenatal infection is a risk factor for brain and behaviour changes relevant to schizophrenia and autism

TitleEvidence that prenatal infection is a risk factor for brain and behaviour changes relevant to schizophrenia and autism
Authors
Issue Date2009
PublisherFrontiers Research Foundation
Citation
The 41st Meeting of the European Brain and Behaviour Society (EBBS) and the 23rd Meeting of the Hellenic Society for Neuroscience (HSfN), Rhodes Island, Greece, 13-18 September 2009. In Frontiers in Behavioral Neuroscience, 2009 How to Cite?
AbstractMaternal infection during pregnancy increases risk of serious psychiatric disorders in the offspring such as schizophrenia and autism, in the offspring. Environmental influences are implicated in the development of ventriculomegaly in schizophrenia, the most consistent brain markers for schizophrenia in man. We hypothesized that maternal infection during pregnancy is an environmental risk factor for ventricular enlargement in offspring. To address this hypothesis we used an mouse model of maternal immune activation (MIA) by the viral mimic PolyI:C administered in early (day 9) or late (day 17) gestation. Automated voxel-based morphometry (VBM) of in-vivo MRI data mapped cerebrospinal fluid across the whole brain. Manual region-of-interest tracing of lateral ventricles confirmed close overlap in ventriclar volumes extracted by each technique (Dice co-efficient = 0.93). We evaluated the behavioural and pharmacological impact of the prenatal exposure using the prepulse inhibition paradigm and an amphetamine challenge in the same mice. Maternal immune activation, in early but not late gestation, caused significant enlargement of lateral ventricles in adulthood. This early exposure disrupted prepulse inhibition and enhanced amphetamine sensitivity. Immune challenge in late gestation caused significant expansion of 4th ventricle volume and a lesser degree of amphetamine potentiation. Our findings lend direct support to the hypothesis that early prenatal immune activation exerts a more extensive neurodevelopmental impact in terms of schizophrenia-related brain and behavioral abnormalities compared with immunological insults taking place later in gestation. Such effects are potentially modifiable and deserve close attention in the context of the wider schizophrenia-autism spectrum.
DescriptionPoster Presentation
Persistent Identifierhttp://hdl.handle.net/10722/126784
ISSN

 

DC FieldValueLanguage
dc.contributor.authorMcAlonan, GMen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorCheung, Cen_HK
dc.contributor.authorWei, Ren_HK
dc.contributor.authorChua, SEen_HK
dc.contributor.authorSham, PCen_HK
dc.contributor.authorWu, EXen_HK
dc.date.accessioned2010-10-31T12:48:20Z-
dc.date.available2010-10-31T12:48:20Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 41st Meeting of the European Brain and Behaviour Society (EBBS) and the 23rd Meeting of the Hellenic Society for Neuroscience (HSfN), Rhodes Island, Greece, 13-18 September 2009. In Frontiers in Behavioral Neuroscience, 2009en_HK
dc.identifier.issn1662-5153 (electronic)-
dc.identifier.urihttp://hdl.handle.net/10722/126784-
dc.descriptionPoster Presentation-
dc.description.abstractMaternal infection during pregnancy increases risk of serious psychiatric disorders in the offspring such as schizophrenia and autism, in the offspring. Environmental influences are implicated in the development of ventriculomegaly in schizophrenia, the most consistent brain markers for schizophrenia in man. We hypothesized that maternal infection during pregnancy is an environmental risk factor for ventricular enlargement in offspring. To address this hypothesis we used an mouse model of maternal immune activation (MIA) by the viral mimic PolyI:C administered in early (day 9) or late (day 17) gestation. Automated voxel-based morphometry (VBM) of in-vivo MRI data mapped cerebrospinal fluid across the whole brain. Manual region-of-interest tracing of lateral ventricles confirmed close overlap in ventriclar volumes extracted by each technique (Dice co-efficient = 0.93). We evaluated the behavioural and pharmacological impact of the prenatal exposure using the prepulse inhibition paradigm and an amphetamine challenge in the same mice. Maternal immune activation, in early but not late gestation, caused significant enlargement of lateral ventricles in adulthood. This early exposure disrupted prepulse inhibition and enhanced amphetamine sensitivity. Immune challenge in late gestation caused significant expansion of 4th ventricle volume and a lesser degree of amphetamine potentiation. Our findings lend direct support to the hypothesis that early prenatal immune activation exerts a more extensive neurodevelopmental impact in terms of schizophrenia-related brain and behavioral abnormalities compared with immunological insults taking place later in gestation. Such effects are potentially modifiable and deserve close attention in the context of the wider schizophrenia-autism spectrum.-
dc.languageengen_HK
dc.publisherFrontiers Research Foundation-
dc.relation.ispartofFrontiers in Behavioral Neuroscience-
dc.titleEvidence that prenatal infection is a risk factor for brain and behaviour changes relevant to schizophrenia and autismen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hken_HK
dc.identifier.emailLi, Q: ciqi@hkucc.hku.hken_HK
dc.identifier.emailCheung, C: charlton@hkucc.hku.hken_HK
dc.identifier.emailWei, R: weiranapply@hotmail.comen_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.authorityMcAlonan, GM=rp00475en_HK
dc.identifier.authorityChua, SE=rp00438en_HK
dc.identifier.authoritySham, PC=rp00459en_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.3389/conf.neuro.08.2009.09.228-
dc.identifier.hkuros172416en_HK
dc.identifier.hkuros178109-
dc.description.otherThe 41st Meeting of the European Brain and Behaviour Society (EBBS) and the 23rd Meeting of the Hellenic Society for Neuroscience (HSfN), Rhodes Island, Greece, 13-18 September 2009. In Frontiers in Behavioral Neuroscience, 2009-

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