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Moreover, there is evidence that conditions <jats:italic>in utero<\/jats:italic>, either alone or in concert with genetic factors, may alter neurodevelopment and lead to an increased risk for schizophrenia. There has been progress in identifying genetic loci and environmental exposures that increase risk, but there are still considerable gaps in our knowledge. Furthermore, very little is known about the specific neurodevelopmental mechanisms upon which genetics and the environment act to increase disposition to developing schizophrenia in adulthood. Vitamin D deficiency during the perinatal period has been hypothesized to increase risk for schizophrenia in humans. The developmental vitamin D (<jats:styled-content style=\"fixed-case\">DVD<\/jats:styled-content>) deficiency hypothesis of schizophrenia arises from the observation that disease risk is increased in individuals who are born in winter or spring, live further from the equator or live in urban vs. rural settings. These environments result in less exposure to sunlight, thereby reducing the initial steps in the production of vitamin D. Rodent models have been developed to characterize the behavioral and developmental effects of <jats:styled-content style=\"fixed-case\">DVD<\/jats:styled-content> deficiency. This review focuses on these animal models and discusses the current knowledge of the role of <jats:styled-content style=\"fixed-case\">DVD<\/jats:styled-content> deficiency in altering behavior and neurobiology relevant to schizophrenia.<\/jats:p>","DOI":"10.1111\/gbb.12271","type":"journal-article","created":{"date-parts":[[2015,11,11]],"date-time":"2015-11-11T13:38:42Z","timestamp":1447249122000},"page":"45-61","source":"Crossref","is-referenced-by-count":36,"title":["Developmental vitamin D deficiency and schizophrenia: the role of animal models"],"prefix":"10.1111","volume":"15","author":[{"given":"S. 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