Animal Models of Autism: An Epigenetic and Environmental Viewpoint

Journal of Central Nervous System Disease

Review

Norio Mori¹  Takayuki Manabe²  Keiko Iwata³  Hideo Matsuzaki³  Nori Takei⁴ 

[1] Department of Psychiatry and Neurology, Hamamatsu University School of Medicine, Shizuoka, Japan.;Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University, Aichi, Japan.;Osaka Hamamatsu Joint Research Center for Child Mental Development, Hamamatsu University School of Medicine, Hamamatsu, Japan.;Osaka Hamamatsu Joint Research Center for Child Mental Development, Hamamatsu University School of Medicine, Hamamatsu, Japan.; The Institute of Psychiatry, London, United Kingdom.;

关键词: autism;    environmental factors;    epigenetic processes;    experimental animal models;   

DOI  :  10.4137/JCNSD.S6188

来源: Sage Journals

【 摘 要 】

Autism is a neurodevelopmental disorder of social behavior, which is more common in males than in females. The causes of autism are unknown; there is evidence for a substantial genetic component, but it is likely that a combination of genetic, environmental and epigenetic factors contribute to its complex pathogenesis. Rodent models that mimic the behavioral deficits of autism can be useful tools for dissecting both the etiology and molecular mechanisms. This review discusses animal models of autism generated by prenatal or neonatal environmental challenges, including virus infection and exposure to valproic acid (VPA) or stress. Studies of viral infection models suggest that interleukin-6 can influence fetal development and programming. Prenatal exposure to the histone deacetylase inhibitor VPA has been linked to autism in children, and male VPA-exposed rats exhibit a spectrum of autistic-like behaviors. The experience of prenatal stress produces male-specific behavioral abnormalities in rats. These effects may be mediated by epigenetic modifications such as DNA methylation and histone acetylation resulting in alterations to the transcriptome.

【 授权许可】

CC BY-NC   
© 2010 SAGE Publications.

【 图 表 】

Figure 1.