Exp Neurobiol 2017; 26(1): 11-24
Published online February 28, 2017
© The Korean Society for Brain and Neural Sciences
Suji Ham1,2, Tae Kyoo Kim1,4, Sooyoung Chung3 and Heh-In Im1,2,3*
1Convergence Research Center for Diagnosis, Treatment and Care System of Dementia, Korea Institute of Science and Technology (KIST), Seoul 02792, 2Department of Neuroscience, Korea University of Science and Technology (UST), Daejeon 34113, 3Center for Neuroscience, Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea, 4Department of Biology, Boston University, Boston 02215, USA
Correspondence to: *To whom correspondence should be addressed.
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Addictive drug use or prescribed medicine abuse can cause psychosis. Some representative symptoms frequently elicited by patients with psychosis are hallucination, anhedonia, and disrupted executive functions. These psychoses are categorized into three classifications of symptoms: positive, negative, and cognitive. The symptoms of DIP are not different from the symptoms of schizophrenia, and it is difficult to distinguish between them. Due to this ambiguity of distinction between the DIP and schizophrenia, the DIP animal model has been frequently used as the schizophrenia animal model. However, although the symptoms may be the same, its causes are clearly different in that DIP is acquired and schizophrenia is heritable. Therefore, in this review, we cover several DIP models such as of amphetamine, PCP/ketamine, scopolamine, and LSD, and then we also address three schizophrenia models through a genetic approach with a new perspective that distinguishes DIP from schizophrenia.
Keywords: drug abuse, psychosis, drug induced psychosis, schizophrenia, animal model