期刊
SCIENTIFIC REPORTS
卷 6, 期 -, 页码 -出版社
NATURE RESEARCH
DOI: 10.1038/srep36087
关键词
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资金
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Japan Agency for Medical Research and development, AMED
- Postdoctoral Fellowship for Overseas Researchers of the Japan Society for the Promotion of Science (JSPS) (Tokyo, Japan)
- Grants-in-Aid for Scientific Research [16F14711] Funding Source: KAKEN
Prenatal infection and subsequent abnormal neurodevelopment of offspring is involved in the etiology of schizophrenia. Brain-derived neurotrophic factor (BDNF) and its high affinity receptor, tropomyosin receptor kinase B (TrkB) signaling plays a key role in the neurodevelopment. Pregnant mice exposed to polyriboinosinic-polyribocytidylic acid [poly(I: C)] causes schizophrenia-like behavioral abnormalities in their offspring at adulthood. Here we found that the juvenile offspring of poly(I: C)-treated mice showed cognitive deficits, as well as reduced BDNF-TrkB signaling in the prefrontal cortex (PFC). Furthermore, the adult offspring of poly(I: C)-treated mice showed cognitive deficits, prepulse inhibition (PPI) deficits, reduced BDNF-TrkB signaling, immunoreactivity of parvalbumin (PV) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1 alpha) in the prelimbic (PrL) of medial PFC and CA1 of hippocampus. Supplementation of a TrkB agonist 7,8-dihydroxyflavone (1 mg/mL in drinking water) during juvenile and adolescent stages could prevent these behavioral abnormalities, reduced BDNFTrkB signaling in PFC and CA1, and immunoreactivity of PV and PGC-1 alpha in the PrL of medial PFC and CA1 in the adult offspring from poly(I: C)-treated mice. These findings suggest that early intervention by a TrkB agonist in subjects with ultra-high risk for psychosis may reduce the risk of subsequent transition to schizophrenia.
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