2014 Fiscal Year Final Research Report
Prenatal origin of the risk of mental disorders caused by the defects of maternal-fetal signal relay
Project/Area Number |
24659512
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Embryonic/Neonatal medicine
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Research Institution | Kanazawa Medical University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 大脳皮質 / 白血病抑制因子 / 妊娠 / 胎盤 / 炎症 |
Outline of Final Research Achievements |
Effects of maternal immune activation (MIA) induced by Polyinosinic:polycytidylic acid (Poly I:C) administration (4 mg or 20 mg/kg BW) into pregnant mice were investigated. The MIA-dams demonstrated that alteration of maternal serum IL-6 level was correlated with Poly I: C in a dose dependent manner. However, leukemia inhibitory factor (LIF) level of cerebrospinal fluid and adrenocorticotropic hormone (ACTH) in serum in embryos were decreased by injection of Poly I:C at 20 mg/kg BW into dams. In addition, the proliferating neural stem/progenitor cells and the post mitotic neurons in the dorsal cerebrum were decreased in number by injection of Poly I:C at 20 mg/kg BW into dams. The dorsal cerebrum of embryos with administration of LIF (5μg;g/kg BW) into dams exhibited that 14 of the top 20 up-regulated genes are the autism-related genes, suggesting that the interference of maternal-fetal LIF signaling relay by MIA results in the prenatal risk of autism.
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Free Research Field |
発生学
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