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dc.contributor.authorHam, Suji-
dc.contributor.authorKim, Tae Kyoo-
dc.contributor.authorSooyoung Chung-
dc.contributor.authorIm, Heh-In-
dc.date.accessioned2024-01-20T02:30:23Z-
dc.date.available2024-01-20T02:30:23Z-
dc.date.created2021-09-01-
dc.date.issued2017-02-
dc.identifier.issn1226-2560-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/123139-
dc.description.abstractAddictive 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.-
dc.languageEnglish-
dc.publisherKOREAN SOC BRAIN & NEURAL SCIENCE, KOREAN SOC NEURODEGENERATIVE DISEASE-
dc.subjectESCALATING DOSAGE SCHEDULE-
dc.subjectPREPULSE INHIBITION-
dc.subjectLATENT INHIBITION-
dc.subjectPREFRONTAL CORTEX-
dc.subjectGENE-EXPRESSION-
dc.subjectWORKING-MEMORY-
dc.subjectRECEPTOR HYPOFUNCTION-
dc.subjectPYRAMIDAL NEURONS-
dc.subjectINDUCED DEFICITS-
dc.subjectANIMAL-MODEL-
dc.titleDrug Abuse and Psychosis: New Insights into Drug- induced Psychosis-
dc.typeArticle-
dc.identifier.doi10.5607/en.2017.26.1.11-
dc.description.journalClass1-
dc.identifier.bibliographicCitationEXPERIMENTAL NEUROBIOLOGY, v.26, no.1, pp.11 - 24-
dc.citation.titleEXPERIMENTAL NEUROBIOLOGY-
dc.citation.volume26-
dc.citation.number1-
dc.citation.startPage11-
dc.citation.endPage24-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.identifier.kciidART002202477-
dc.identifier.wosid000406862000002-
dc.identifier.scopusid2-s2.0-85013853770-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaResearch & Experimental Medicine-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeReview-
dc.subject.keywordPlusESCALATING DOSAGE SCHEDULE-
dc.subject.keywordPlusPREPULSE INHIBITION-
dc.subject.keywordPlusLATENT INHIBITION-
dc.subject.keywordPlusPREFRONTAL CORTEX-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusWORKING-MEMORY-
dc.subject.keywordPlusRECEPTOR HYPOFUNCTION-
dc.subject.keywordPlusPYRAMIDAL NEURONS-
dc.subject.keywordPlusINDUCED DEFICITS-
dc.subject.keywordPlusANIMAL-MODEL-
dc.subject.keywordAuthordrug abuse-
dc.subject.keywordAuthorpsychosis-
dc.subject.keywordAuthordrug induced psychosis-
dc.subject.keywordAuthorschizophrenia-
dc.subject.keywordAuthoranimal model-
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