Human epidemiological studies have indicated an association between infection during pregnancy and an increased risk of neurodevelopmental disorders such as schizophrenia in offspring. As infections arising from various causes have a similar debilitating effect in later life, it is thought that the maternal response, common to most infections, may be the critical factor altering fetal brain development. In this chapter, we discuss various animal models of prenatal exposure to an infection, that have aimed to cause neurobiological, pharmacological and behavioral abnormalities in offspring comparable to those seen in schizophrenic patients. We propose that one such model, the prenatal treatment with the viral mimetic, polyriboinosinic-polyribocytidylic acid (Poly I:C) successfully demonstrates critical features of the human disorder. Therefore, this model is ideal to further investigate the neurodevelopmental basis of schizophrenia and, importantly, may provide a useful tool for testing treatment strategies.