Human epidemiological studies have provided compelling evidence that the risk of developing schizophrenia is enhanced by prenatal maternal infection with viral or bacterial pathogens. Recent experimentation in rodents has yielded additional support for a causal relationship between prenatal immune challenge and the emergence of psychosis-related abnormalities in brain and behavior in later life. Based on these associations, developing a reliable, predictive animal model of psychiatric disorder, such as schizophrenia, is essential for us to study the neurobiological mechanisms and for the development of novel drugs with improved therapeutic efficacy. Therefore the goal of the article was to review the contribution of prenatal immune challenge (PIC) in pregnant rodent models, especially the one using the viral-mimetic particle polyriboinosinic-polyribocytidylic acid (poly-I:C) to the study of etiology, biological basis and treatment of schizophrenia. Available web databases (PubMed and ISI web of science) for original studies published in the last 10 years (From 2003 to 2013) concerning animal model of PIC, focusing on inducing by poly-I:C were searched in the article. The neurodevelopmental model, challenged by the viral mimetic poly-I:C, not only exerts behavioral effects on sensorimotor gating deficits, latent inhibition disruption, impaired object recognition memory and social behavior dysfunction in adult rat offspring, but further produces effects of postpubertal emergence of enhanced sensitivity to MK-801 and amphetamine-induced hyperlocomotion, all those effects are followed with morphofunctional alterations in the hippocampus and the entorhinal cortex in adult offspring. Several gene expression changes related to the developmental course of dopaminergic neurons, including the sonic hedgehog (ShhN) and fibroblastic growth factor 8 (FGF-8), as well as transcription factors like nuclear receptor related 1 protein (Nurr1) and pituitary homeobox 3 (Pitx3) can also be confirmed in the neurodevelopmental model. The ShhN and FGF-8 genes, as well as the transcription factors Nurr1 and Pitx3, are essential for the generation, differentiation, and maintenance of midbrain dopamine (DA) cells during embryonic development. Besides that, chronic injection of antipsychotics (haloperidol and clozapine) or the antidepressant fluoxetine during periadolescence blocked the onset of psychotic symptoms in animals predisposed to schizophrenia by PIC. The PIC model challenged by the viral mimetic poly-I:C enables the study of antipsychotic drugs in a preventive (prenatal life and prodrome) and therapeutic approach. We thus conclude that the neurodevelopmental models of schizophrenia, challenged by the viral mimetic poly-I:C, are characterized by a high level of face, construct and predictive validity, including intrinsic etiological significance to the disorder. It is able to mimic the positive and negative/cognitive dimensions of schizophrenia, depending on the gestation time window of the administration of poly-I:C. The model resembles the neurobiology and etiology of schizophrenia and has good predictive value. In conclusion, this model is a robust tool for the identification of novel molecular targets during prenatal life, adolescence and adulthood that might contribute to the development of preventive and/or treatment strategies for schizophrenia, also presenting biosafety as compared to viral infection models. One limitation of this model is the incapacity to model the full spectrum of immune responses normally induced by viral exposure.