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Neuronal and behavioral pathology in a maternal immune activation rodent model of schizophrenia

https://repo.qst.go.jp/records/70596
https://repo.qst.go.jp/records/70596
ddecb357-5360-4be1-ad5d-854ee50a2cd8
Item type 会議発表用資料 / Presentation(1)
公開日 2011-11-01
タイトル
タイトル Neuronal and behavioral pathology in a maternal immune activation rodent model of schizophrenia
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Oh-Nishi, Arata

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WEKO 693369

Oh-Nishi, Arata

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et.al

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WEKO 693370

et.al

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大西 新

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WEKO 693371

en 大西 新

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内容記述タイプ Abstract
内容記述 Schizophrenia is characterized by disturbances of thoughts, perception, cognition and volition. It is reported that about 1% of the world population becomes morbid with schizophrenia. However, the etiology of schizophrenia is not well known. Recently, it has been suggested that maternal immune activation increases the risk of psychiatric disorders such as schizophrenia in offspring. Here we investigated whether maternal immune activation produces schizophreniform neuronal and behavioral dysfunction in a rat model. We gave double-stranded RNA polyriboinosinic-polyribocytidilic acid (Poly I:C) (0.4mg/kg/day, I.P.) to pregnant rats on gestation days 15-18, which led to increased IL-6, TNF-alpha and IL-1beta but not IL-2 and IL-10 in the maternal serums 3 hours after injection. We then investigated the neuronal and behavioral pathology of mature offspring of the Poly I:C-treated dams. Using positron emission tomography, we found that dopamine D2/D3 receptor-specific ligand binding potential was significantly decreased in the medial prefrontal cortex (mPFC) in mature offspring of Poly I:C-treated dams (P<0.003), and the number of Parvalbumin-positive cells (P<0.005) but not NeuN-positive cells was reduced. Additionally, abnormal cognitive and/or emotional behavior was observed in these mature offspring by open field test. It has been reported that mPFC dysfunction and abnormal cognitive function are typical phenotypes in schizophrenia patients. In this context, the results indicate a high degree of homology between the rodent model of maternal immune activation pathology and schizophrenia patients. We suggest that maternal immune activation might represent convincing pathoetiology of non-inherited schizophrenia.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 第34回日本神経科学大会
発表年月日
日付 2011-09-17
日付タイプ Issued
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