WEKO3
インデックスリンク
アイテム
グルタミン酸神経毒性と内因性神経保護物質
https://fukuyama-u.repo.nii.ac.jp/records/6930
https://fukuyama-u.repo.nii.ac.jp/records/6930c3bb7bbc-8190-4fdc-821e-f071e81db0ee
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
KJ00005784483.pdf (1.6 MB)
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| Item type | 紀要論文(ELS) / Departmental Bulletin Paper(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 1995-01-01 | |||||
| タイトル | ||||||
| タイトル | グルタミン酸神経毒性と内因性神経保護物質 | |||||
| タイトル | ||||||
| タイトル | Glutamate neurotoxicity and endogenous neuroprotective substance | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | jpn | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | departmental bulletin paper | |||||
| ページ属性 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | P(論文) | |||||
| 記事種別(日) | ||||||
| 値 | 総説 | |||||
| 記事種別(英) | ||||||
| 言語 | en | |||||
| 値 | Review | |||||
| 著者名(日) |
田村, 豊
× 田村, 豊× 塩見, 浩人 |
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| 著者名よみ | ||||||
| 識別子Scheme | WEKO | |||||
| 識別子 | 34979 | |||||
| 姓名 | タムラ, ユタカ | |||||
| 著者名よみ | ||||||
| 識別子Scheme | WEKO | |||||
| 識別子 | 34980 | |||||
| 姓名 | シオミ, ヒロヒト | |||||
| 著者名(英) | ||||||
| 識別子Scheme | WEKO | |||||
| 識別子 | 34981 | |||||
| 姓名 | TAMURA, Yutaka | |||||
| 言語 | en | |||||
| 著者名(英) | ||||||
| 識別子Scheme | WEKO | |||||
| 識別子 | 34982 | |||||
| 姓名 | SHIOMI, Hirohito | |||||
| 言語 | en | |||||
| 著者所属(日) | ||||||
| 値 | 福山大学 | |||||
| 著者所属(日) | ||||||
| 値 | 福山大学 | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | FUKUYAMA UNIVERSITY | |||||
| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | FUKUYAMA UNIVERSITY | |||||
| 抄録(英) | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Glutamate is well known as an excitatory neurotransmitter in the vertebrate central nervous system (CNS). Recently, glutamate is also postulated to play an important role in the pathogenesis of the neuronal cell loss that is associated with several neurological disease states in the CNS. Glutamate neurotoxicity in the cultured cortical neurons is mediated by nitric oxide(NO). As the excitatory action of glutamate is regulated by other neurotransmitters, the neurotoxic action of glutamate may be affected by other endogenous substances. We have previously found that cholecystokinin(CCK) prevented glutamate neurotoxicity in the cultured cortical neurons. The evidence has suggested that CCKB receptor stimulation causes suppression of a step in NO formation triggered by N-methyl-D-aspartate(NMDA) receptor activation. CCK may have a role to promote cell survival in the life-regulatory function of the CNS. This review mainly discusses the mechanisms of glutamate neurotoxicity and CCK-induced protection against glutamate neurotoxicity. | |||||
| 雑誌書誌ID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AN10064550 | |||||
| 書誌情報 |
福山大学薬学部研究年報 en : Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University 巻 13, p. 16-37, 発行日 1995 |
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