Prenatal viral infection in mouse causes differential expression of genes in brains of mouse progeny: A potential animal model for schizophrenia and autism

被引:120
作者
Fatemi, SH
Pearce, DA
Brooks, AI
Sidwell, RW
机构
[1] Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA
[2] Univ Rochester, Sch Med, Ctr Aging & Dev Biol, Dept Biochem & Biophys,Dept Neurol, Rochester, NY USA
[3] Univ Rochester, Sch Med, Dept Environm Med, Ctr Funct Genom, Rochester, NY USA
[4] Utah State Univ, Logan, UT 84322 USA
关键词
human influenza; mouse; brain; autism; schizophrenia; DNA microarray;
D O I
10.1002/syn.20162
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Schizophrenia and autism are neurodevelopmental disorders with genetic and environmental etiologies. Prenatal viral infection has been associated with both disorders. We investigated the effects of prenatal viral infection on gene regulation in offspring of Balb-c mice using microarray technology. The results showed significant upregulation of 21 genes and downregulation of 18 genes in the affected neonatal brain homogenates spanning gene families affecting cell structure and function, namely, cytosolic chaperone system, HSC70, Bicaudal D, aquaporin 4, carbonic anhydrase 3, glycine receptor, norepinephrine transporter, and myelin basic protein. We also verified the results using QPCR measurements of selected mRNA species. These results show for the first time that prenatal human influenza viral infection on day 9 of pregnancy leads to alterations in a subset of genes in brains of exposed offspring, potentially leading to permanent changes in brain structure and function. (c) 2005 Wiley-Liss, Inc.
引用
收藏
页码:91 / 99
页数:9
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