Transgenic Mouse Offers a Window on Gene/Environment Interplay: Prenatal Infection Alters Behavior in Genetically Vulnerable

Experiments in transgenic mice have provided a novel glimpse of how a prenatal infection could interact with a specific gene variant to cause behavioral and neurologic changes in adults that mirror those seen in major psychiatric disease. The mouse model used offers a means to explore gene/environment interactions and to identify both the mechanisms involved and critical periods of vulnerability.

Research has established that the risk of developing a psychiatric illness and the features of the illness are the outcome of interactions between the environment and genes. Understanding the details of these interactions is a complex task, however. Many genes shape brain development and function, and gene function is in turn influenced by myriad environmental factors unfolding across a lifespan.

Genetic technology has made it possible to create model animals that carry risk genes, providing a way to focus on how single genes or mutations shape function and how specific environmental factors alter it.

This Study
Scientists at the Johns Hopkins University School of Medicine in Baltimore led by Mikhail Pletnikov developed the mouse model used in this study by inserting a gene with a mutation known to be associated in humans with schizophrenia, depression, and bipolar disorder. They used a technique that allows them to turn the gene on and off at desired time points during brain development. In earlier research, mice with the gene, mhDISC1 (mutant human disrupted-in-schizophrenia-1) showed effects on social behavior and mood which differed depending on the sex of the mice, and the age at which the gene was active…….

NIMH Press Office

Reference: Abazyan, B., Nomura, J., Kannan, G., Ishizuka, K., Tamashiro, K.L., Nucifora, F., Pogorelov, V., Ladenheim, B., Yang, C., Krasnova, I.N., Cadet, J.L., Pardo, C., Mori, S., Kamiya, A., Vogel, M.W., Sawa, A., Ross, C.A., and Pletnikov, M.V. Prenatal interaction of mutant DISC1 and immune activation produces adult psychopathology. Biological Psychiatry 2010;68:1172-1181.

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