2004 Fiscal Year Final Research Report Summary
The mechanism for the effects of atypical antipsychotics on the cognitive dysfunction of schizophreniavia the modulation of the function of the neuronal network
| Project/Area Number |
14370287
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
KOYAMA Tsukasa Hokkaido Univ., Grad.School of medicine, Professor, 大学院・医学研究科, 教授 (10113557)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUMI Ichirou Hokkaido Univ Hospital, Lecturer, 病院・講師 (30250426)
ABEKAWA Tomihiro Hokkaido Univ Hospital, Assistant Professor, 病院・助手 (80301901)
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| Project Period (FY) |
2002 – 2004
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| Keywords | schizophrenia / cognitive dysfunction / atypical antipsychotics / prefrontal cortex |
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| Research Abstract |
Clarifying the pathogenesis and the mechanism for the treatment of cognitive dysfunction of schizophrenia is important, because this dysfunction induces serious social dysfunction in patients with schizophrenia.
Phencyclidine-induced increases in glutamate levels in the prefrontal cortex and hyperlocomotion were blocked by 5-HT2A receptor antagonist, an atypical antipsychotic, dozapine. Lesioning the mediodortsal thalamus, which projects the glutamatengic neuronal terminals to the prefrontal cortex, enhanced the behavioral and neurochemical changes of NMDA receptor antagonist, MK-801. Chronic administration of an another atypical antipsychotic, olanzapine increased protein level of dopamine D1 receptors in the prefrontal cortex, enhanced working memory of rats.
Therefore, atypical antipsychotics, which can enhance the function of NMDA receptor and dopamine D1 receptor in the prefrontal cortex, may have a potential for improving the cognitive dysfunction of schizophrenia.
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Research Products
(13 results)
