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[PolyI:C-induced neurodevelopmental animal model for schizophrenia].

Daisuke Ibi1, Taku Nagai, Toshitaka Nabeshima

  • 1Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Nihon Shinkei Seishin Yakurigaku Zasshi = Japanese Journal of Psychopharmacology
|January 20, 2012
PubMed
Summary

Maternal immune activation during neurodevelopment, using polyI:C exposure in mice with DISC1 gene variations, can lead to schizophrenia-like behaviors in adulthood, highlighting gene-environment interactions in disease etiology.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Genetics

Background:

  • Schizophrenia affects ~1% of the population, presenting with positive, negative, and cognitive symptoms.
  • Genetic factors (e.g., DISC1) and environmental insults (e.g., prenatal infection) are implicated in schizophrenia development.
  • Gene-environment interactions are proposed as a key factor in schizophrenia etiology.

Purpose of the Study:

  • To investigate the role of gene-environment interactions in schizophrenia development.
  • To establish a validated animal model for studying schizophrenia etiology.
  • To examine how maternal immune activation influences neurodevelopment and adult behavior.

Main Methods:

  • Utilized transgenic mice expressing a dominant-negative form of DISC1 (DN-DISC1).
  • Administered polyriboinosinic-polyribocytidylic acid (polyI:C) to neonatal DN-DISC1 mice to simulate maternal immune activation.
  • Assessed behavioral and neurochemical abnormalities in adult offspring.

Main Results:

  • Neonatal polyI:C injection in DN-DISC1 mice induced schizophrenia-like behavioral abnormalities in adulthood.
  • This model demonstrated a clear link between genetic susceptibility (DN-DISC1) and environmental insult (polyI:C).
  • The polyI:C-treated DN-DISC1 mice exhibited phenotypic changes consistent with schizophrenia.

Conclusions:

  • PolyI:C-treated DN-DISC1 mice serve as a validated animal model for schizophrenia research.
  • Gene-environment interactions during neurodevelopment are crucial for adult phenotypic expression in schizophrenia.
  • This model facilitates further investigation into the molecular mechanisms underlying schizophrenia.