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Neural Plasticity
Volume 2012, Article ID 832757, 12 pages
Review Article

Effects of Antipsychotics on Dentate Gyrus Stem Cell Proliferation and Survival in Animal Models: A Critical Update

1Institute of Biochemistry and Cell Biology, University of Magdeburg, Leipziger Straße 44, 39120 Magdeburg, Germany
2Institute of Psychiatry, King's College London, 5th Floor, Main Building, P.O. Box 63, De Crespigny Park, London SE5 8AF, UK
3Institute of Pharmacology and Toxicology, University of Magdeburg, Leipziger Straße 44, 39120 Magdeburg, Germany

Received 12 June 2012; Revised 19 September 2012; Accepted 20 September 2012

Academic Editor: Chitra D. Mandyam

Copyright © 2012 Gerburg Keilhoff et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Schizophrenia is a complex psychiatric disorder. Although a number of different hypotheses have been developed to explain its aetiopathogenesis, we are far from understanding it. There is clinical and experimental evidence indicating that neurodevelopmental factors play a major role. Disturbances in neurodevelopment might result in alterations of neuroanatomy and neurochemistry, leading to the typical symptoms observed in schizophrenia. The present paper will critically address the neurodevelopmental models underlying schizophrenia by discussing the effects of typical and atypical antipsychotics in animal models. We will specifically discuss the vitamin D deficiency model, the poly I:C model, the ketamine model, and the postnatal ventral hippocampal lesion model, all of which reflect core neurodevelopmental issues underlying schizophrenia onset.