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Conference Paper: Prenatal exposure of mice to a maternal immune challenge leads to neurobiological changes in offspring relevant to schizophrenia

TitlePrenatal exposure of mice to a maternal immune challenge leads to neurobiological changes in offspring relevant to schizophrenia
Authors
KeywordsBiology
Biochemistry medical sciences
Psychiatry and neurology
Issue Date2009
PublisherBlackwell Publishing Ltd.
Citation
The 22nd Biennial Meeting of the ISN/APSN Joint Meeting, Busan, South Korea, 23-28 August 2009. In Journal of Neurochemistry, 2009, v. 110 suppl. s2, p. 174-175 How to Cite?
AbstractMaternal infection during pregnancy increases the risk of serious neuropsychiatric disorders, such as schizophrenia and autism, in the offspring. MRI in patient populations shows white matter abnormalities and postmortem microarray and qPCR studies in the literature point to gene expression alterations in oligodendrocytes. We hypothesized that viral infection during pregnancy is an environmental risk factor for both the altered expression of genes regulating white matter development and subsequent ventricular enlargement in offspring. We used a mouse model of maternal immune activation (MIA) by the viral mimic poly(I : 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 ventricular volumes extracted by each technique (Dice coefficient = 0.93). We evaluated the behavioral and pharmacological impact of the prenatal exposure by using the prepulse inhibition paradigm and an amphetamine challenge in the same mice. Gene expression patterns of several white matter markers were characterized by in situ hybridization and immunohistochemistry. 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 fourth-ventricle volume and a lesser degree of amphetamine potentiation.
DescriptionThis is the Special Issue of Abstracts for the 22nd Biennial Meeting of the ISN/APSN Joint Meeting
Poster Session - TH03 Effects of perinatal stress: abstract no. TH03-11
Persistent Identifierhttp://hdl.handle.net/10722/126786
ISSN
2015 Impact Factor: 3.842
2015 SCImago Journal Rankings: 2.021

 

DC FieldValueLanguage
dc.contributor.authorWong, NKen_HK
dc.contributor.authorLi, Qen_HK
dc.contributor.authorCheung, Cen_HK
dc.contributor.authorWei, Ren_HK
dc.contributor.authorHui, ESen_HK
dc.contributor.authorWu, EXen_HK
dc.contributor.authorMcAlonan, GMen_HK
dc.date.accessioned2010-10-31T12:48:27Z-
dc.date.available2010-10-31T12:48:27Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 22nd Biennial Meeting of the ISN/APSN Joint Meeting, Busan, South Korea, 23-28 August 2009. In Journal of Neurochemistry, 2009, v. 110 suppl. s2, p. 174-175en_HK
dc.identifier.issn0022-3042en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126786-
dc.descriptionThis is the Special Issue of Abstracts for the 22nd Biennial Meeting of the ISN/APSN Joint Meeting-
dc.descriptionPoster Session - TH03 Effects of perinatal stress: abstract no. TH03-11-
dc.description.abstractMaternal infection during pregnancy increases the risk of serious neuropsychiatric disorders, such as schizophrenia and autism, in the offspring. MRI in patient populations shows white matter abnormalities and postmortem microarray and qPCR studies in the literature point to gene expression alterations in oligodendrocytes. We hypothesized that viral infection during pregnancy is an environmental risk factor for both the altered expression of genes regulating white matter development and subsequent ventricular enlargement in offspring. We used a mouse model of maternal immune activation (MIA) by the viral mimic poly(I : 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 ventricular volumes extracted by each technique (Dice coefficient = 0.93). We evaluated the behavioral and pharmacological impact of the prenatal exposure by using the prepulse inhibition paradigm and an amphetamine challenge in the same mice. Gene expression patterns of several white matter markers were characterized by in situ hybridization and immunohistochemistry. 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 fourth-ventricle volume and a lesser degree of amphetamine potentiation.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd.-
dc.relation.ispartofJournal of Neurochemistryen_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subjectBiology-
dc.subjectBiochemistry medical sciences-
dc.subjectPsychiatry and neurology-
dc.titlePrenatal exposure of mice to a maternal immune challenge leads to neurobiological changes in offspring relevant to schizophreniaen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLi, Q: ciqi@hkucc.hku.hken_HK
dc.identifier.emailCheung, C: charlton@hkucc.hku.hken_HK
dc.identifier.emailWu, EX: ewu@eee.hku.hken_HK
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hken_HK
dc.identifier.authorityCheung, C=rp01574en_HK
dc.identifier.authorityWu, EX=rp00193en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1471-4159.2009.06242.x-
dc.identifier.hkuros175961en_HK
dc.identifier.volume110en_HK
dc.identifier.issuesuppl. s2-
dc.identifier.spage174en_HK
dc.identifier.epage175en_HK
dc.publisher.placeUnited Kingdom-
dc.description.otherThe 22nd Biennial Meeting of the ISN/APSN Joint Meeting, Busan, South Korea, 23-28 August 2009. In Journal of Neurochemistry, 2009, v. 110 suppl. s2, p. 174-175-

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