{"created":"2023-06-20T15:28:27.475045+00:00","id":7528,"links":{},"metadata":{"_buckets":{"deposit":"3cc3563a-ba3f-465d-ad8f-128d36711cc2"},"_deposit":{"created_by":3,"id":"7528","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"7528"},"status":"published"},"_oai":{"id":"oai:ouj.repo.nii.ac.jp:00007528","sets":["470:394:437"]},"author_link":["9576","9577"],"item_10002_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2010-03-23","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"23","bibliographicPageStart":"1","bibliographicVolumeNumber":"27","bibliographic_titles":[{"bibliographic_title":"放送大学研究年報"},{"bibliographic_title":"Journal of the Open University of Japan","bibliographic_titleLang":"en"}]}]},"item_10002_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"　統合失調症は1％近い発症危険率をもち、世界的に広く認められる代表的な精神疾患である。思春期・青年期に好発し、多彩な精神症状を呈しつつ再燃を繰り返しながら慢性的に経過するもので、クレペリン以来、進行性かつ予後不良の疾患とされてきた。かつて統合失調症には有効な治療法が存在しなかったが、1952年に最初の抗精神病薬であるクロルプロマジンが開発されて以来、薬物療法が長足の進歩を遂げた。その結果、予後は劇的に改善され、既に重症疾患ではなくなったとの認識があるが、わが国では精神科入院者数の60％以上を依然として統合失調症の患者が占めており、その中には少なからぬ社会的入院者が含まれている。\n　統合失調症の発症機序に関しては、抗精神病薬の作用機序や覚醒剤精神病の知見などにもとづいて、ドーパミン神経伝達の過活動を想定するドーパミン仮説が有力視されてきたが、陰性症状や慢性化した陽性症状には抗精神病薬の効果が乏しいことなどから、同仮説の限界も指摘されている。ドーパミン仮説を補完しより包括的な疾患理解と治療方略を指向するものとして、統合失調症脳内におけるグルタミン酸神経伝達の低活動を想定するグルタミン酸仮説が挙げられる。本稿ではグルタミン酸仮説の根拠を紹介するとともに、統合失調症死後脳におけるグルタミン酸受容体研究の成果を紹介するとともに、その課題と将来性について論じた。また、死後脳研究におけるグルタミン酸受容体増加所見の分布を踏まえ、前頭連合野と頭頂連合野の変調が統合失調症の症状形成に関与することを推定し、「統合失調症の連合野仮説」の可能性について検討した。解決すべき課題は多く残されているものの、今後の研究の方向を決定するうえで「連合野仮説」は有益な示唆を含むものと考えられる。","subitem_description_type":"Abstract"}]},"item_10002_source_id_11":{"attribute_name":"書誌レコードID","attribute_value_mlt":[{"subitem_source_identifier":"AN10019636","subitem_source_identifier_type":"NCID"}]},"item_10002_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0911-4505","subitem_source_identifier_type":"ISSN"}]},"item_10002_textarea_25":{"attribute_name":"抄録（英）","attribute_value_mlt":[{"subitem_textarea_language":"en","subitem_textarea_value":"　Schizophrenia has long been taken as a chronic progressive illness with a poor prognosis, which is observed across the world with a morbidity rate of nearly 1％. There had not been an effective therapeutic method for ameliorating schizophrenic symptoms until 1952, when the first antipsychotic agent chlorpromazine was introduced to the field of psychiatry with a dramatic effect on the patients. Since then the pharmacotherapy of schizophrenia improved so rapidly and profoundly that the prognosis does not seem to be poor any more. In Japan, however, schizophrenic patients occupy 60％ of the psychiatric inpatients and many of them are kept hospitalized due to the social conditions such as the lack of habitation and a social support network.\n　In terms of the pathological mechanisms, the dopamine hypothesis which implies a dopaminergic hyperactivity in the brain of schizophrenics has been accepted widely. The hypothesis has been supported strongly by the fact that the anti-dopaminergic agents are effective in ameliorating the positive symptoms and in preventing the relapse as well as by the observation of the metamphetamine-induced psychosis which mimics schizophrenic positive symptoms by enhancing the release of dopamine in the brain. It also has a limitation since the anti-dopaminergic agents are not effective in treating schizophrenic negative symptoms and other chronic symptoms. Among the candidates for a more comprehensive theory of schizophrenia, the glutamate hypothesis which implies a hypoactivity in glutamatergic neurotransmission in the cerebral cortex of schizophrenia seems to be a promising one. In this paper the bases for the glutamate hypothesis are introduced and discussed. Specifically, the measurement of glutamate receptors that was performed using postmortem brains of the patients are described. The results included a significant increase in the glutamate receptors in the several cortical fields of the schizophrenic brains, with its distribution strongly implicates the involvement of the two major association fields, the prefrontal and the parietal. As a conclusion, \"the association cortex hypothesis of schizophrenia\" is suggested, which implies a glutamatergic hypoactivity in the associative cortices is involved in the course of schizophrenia."}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"石丸, 昌彦"},{"creatorName":"イシマル, マサヒコ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{"nameIdentifier":"9576","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"Ishimaru, Masahiko","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"9577","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2013-06-14"}],"displaytype":"detail","filename":"27-1.pdf","filesize":[{"value":"4.2 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"27-1","url":"https://ouj.repo.nii.ac.jp/record/7528/files/27-1.pdf"},"version_id":"1e9cfaaa-5905-4b33-9567-0567f8dde414"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"departmental bulletin paper","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"統合失調症小史","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"統合失調症小史"},{"subitem_title":"Schizophrenia : A Historical Review","subitem_title_language":"en"}]},"item_type_id":"10002","owner":"3","path":["437"],"pubdate":{"attribute_name":"公開日","attribute_value":"2013-06-14"},"publish_date":"2013-06-14","publish_status":"0","recid":"7528","relation_version_is_last":true,"title":["統合失調症小史"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2023-06-20T16:19:35.957010+00:00"}