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統合失調症I
Schizophrenia I

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開催日
2010年09月02日(木)
時 間
13:00 - 14:00
会 場
Poster Room 2

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統合失調症様症状を誘発するNMDA受容体遮断薬フェンサイクリジンを全身投与したラットの大脳新皮質における遺伝子発現の発達に伴う変化
Profiling of developmental changes in the gene expression following systemic administration of a schizophrenomimetic NMDA receptor antagonist phencyclidine in the rat neocortex

演題番号 : P1-p06

海野 真一 / Masakazu Umino:1 山本 直樹 / Naoki Yamamoto:1 竹林 裕直 / Hironao Takebayashi:1 海野 麻未 / Asami Umino:1 車地 暁生 / Akeo Kurumaji:1 西川 徹 / Toru Nishikawa:1 

1:東京医科歯科大学大学院 精神行動医科学分野 / Sec Psychiatry Behav Sci, Tokyo Med Dent Univ, Tokyo, JAPAN 

 

Schizophrenic symptoms and their pharmacological models induced by the NMDA type glutamate receptor antagonists are usually observed after the puberty in humans or the weaning period in rats and mice. The development-dependent nature of the onset of schizophrenia and psychotomimetic effects of these drugs can be hypothesized to be associated with the maturation of the brain information processing systems (or the neuron circuits) that are specifically disturbed in schizophrenia or its animal models. Such a mammalian system should be equipped with the molecular cascades that differentially respond to schizophrenomimetics before and after the maturation. We have indeed identified several developmentally regulated a potent NMDA receptor antagonist phencyclidine-inducible genes from the rat or mouse brain regions as the novel candidates for the schizophrenia-related molecules by comparing the gene expression patterns between postnatal days 8 and 50. To get more inclusive insights into the molecular basis of schizophrenia, we have investigated the gene expression profiles after systemic administration of phencyclidine at postnatal days 8, 18, 25 and 50 in the rat neocortex by using a DNA microarray technique that can monitor the expression of approximately 280,000 genes. The profiles were different markedly between the two next postnatal days. Phencyclidine caused an increase in the expression of 24 genes at the four postnatal days while other 62 genes were upregulated only after the critical period around postnatal weeks 3 for the adult-type of phencyclidine-induced abnormal behavior that has been considered to be a model for schizophrenia. These data suggest that the 62 genes showing the critical period-related expressional changes could compose the molecular cascades that might be involved in the pathophysiology of schizophrenia.

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