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DISC1  was discovered in a Scottish pedigree in which a chromosomal translocation that breaks this gene segregates with psychiatric disorders, mainly depression and schizophrenia. Linkage and association studies in diverse populations support  DISC1  as a susceptibility gene to a variety of neuropsychiatric disorders. Many  Disc1  mouse models have been generated to study its neuronal functions. These mouse models display variable phenotypes, some of them relevant to schizophrenia, others to depression. The  Disc1  mouse models are popular genetic models for studying gene-environment interactions in schizophrenia. Five different  Disc1  models have been combined with environmental factors. The environmental stressors employed can be classified as either early immune activation or later social paradigms. These studies cover major time points along the neurodevelopmental trajectory: prenatal, early postnatal, adolescence, and adulthood. Various combinations of molecular, anatomical and behavioral methods have been used to assess the outcomes. Additionally, three of the studies sought to rescue the resulting abnormalities. Here we provide background on the environmental paradigms used, summarize the results of these studies combining  Disc1  mouse models with environmental stressors and discuss what we can learn and how to proceed. A major question is how the genetic and environmental factors determine which psychiatric disorder will be clinically manifested. To address this we can take advantage of the many  Disc1  models available and expose them to the same environmental stressor. The complementary experiment would be to expose the same model to different environmental stressors.  DISC1  is an ideal gene for this approach, since in the Scottish pedigree the same chromosomal translocation results in different psychiatric conditions.

DISC1 mouse models as a tool to decipher gene-environment interactions in psychiatric disorders