Prenatal viral infection of mice at E16 causes changes in gene expression in hippocampi of the offspring

S H Fatemi, Timothy D. Folsom, Teri J. Reutiman, Hao Huang, Kenichi Oishi, Susumu Mori

Research output: Contribution to journalArticlepeer-review

41 Scopus citations


The hippocampus governs memory formation and emotional regulation, and there is widespread evidence of hippocampal dysfunction in psychiatric disorders, including schizophrenia and autism. There is abundant evidence that prenatal viral infection may play a role in the development of these two disorders. In the current study, we have examined gene expression and structural changes of the hippocampi of exposed neonates following maternal infection at embryonic day (E) 16 (middle second trimester). We observed significant changes in gene expression in the offspring at postnatal day (P) 0 (birth), P14 (childhood), and P56 (adulthood), including a number of candidate genes for autism and schizophrenia. qRT-PCR verified the direction and magnitude of change for 5 of the genes from the microarray data set and revealed mRNA changes for additional genes associated with schizophrenia and autism. MRI revealed a decrease in hippocampal volume at P35 (adolescence). Our results demonstrate altered gene expression and reduced hippocampal volume in the offspring following prenatal viral infection at E16.

Original languageEnglish (US)
Pages (from-to)648-653
Number of pages6
JournalEuropean Neuropsychopharmacology
Issue number9
StatePublished - Sep 2009

Bibliographical note

Funding Information:
Funding for this study was provided by the National Institute of Child Health and Human Development (#5R01-HD046589-04). The funding source had no further role in the study design; in the collection, analysis and interpretation of the data; in the writing of the report; and in the decision to submit the paper for publication.


  • Autism
  • DNA microarray
  • Hippocampus
  • Mouse
  • Schizophrenia
  • Viral model


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