To poly(I:C) or not to poly(I:C): Advancing preclinical schizophrenia research through the use of prenatal immune activation models

Urs Meyer*, Joram Feldon

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The neurodevelopmental hypothesis of schizophrenia has been highly influential in shaping our current thinking about modeling the disease in animals. Based on the findings provided by human epidemiological studies, a great deal of recent interest has been centered upon the establishment of neurodevelopmental rodent models in which the basic experimental manipulation takes the form of prenatal exposure to infection and/or immune activation. One such model is based on prenatal treatment with the inflammatory agent poly(I:C) (=polyriboinosinic-polyribocytidilic acid), a synthetic analog of double-stranded RNA. Since its initial establishment and application to basic schizophrenia research, the poly(I:C) model has made a great impact on researchers concentrating on the neurodevelopmental and neuroimmunological basis of complex human brain disorders such as schizophrenia, and as a consequence, the model now enjoys wide recognition in the international scientific community. The present article emphasizes that the poly(I:C) model has gained such impact because it successfully accounts for several aspects of schizophrenia epidemiology, pathophysiology, symptomatology, and treatment. The numerous features of this experimental system make the poly(I:C) model a very powerful neurodevelopmental animal model of schizophrenia-relevant brain disease which is expected to be capable of critically advancing our knowledge of how the brain, following an (immune-associated) triggering event in early life, can develop into a "schizophrenia-like brain" over time. Furthermore, the poly(I:C) model seems highly suitable for the exploration of novel pharmacological and neuro-immunomodulatory strategies for both symptomatic and preventive treatments against psychotic disease, as well as for the identification of neurobiological mechanisms underlying gene-environment and environment-environment interactions presumably involved in the etiology of schizophrenia and related disorders. This article is part of a Special Issue entitled 'Schizophrenia'.

Original languageEnglish
Pages (from-to)1308-1321
Number of pages14
Issue number3
StatePublished - Mar 2012
Externally publishedYes


  • Animal model
  • Cognition
  • Cytokines
  • Dopamine
  • Glutamate
  • Prevention
  • Prodromal


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