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The role of glucocorticoid receptors in the induction and prevention of hippocampal abnormalities in an animal model of posttraumatic stress disorder

https://hiroshima.repo.nii.ac.jp/records/2008720
https://hiroshima.repo.nii.ac.jp/records/2008720
d5b32745-79e4-488a-952d-fa96b02c582a
名前 / ファイル ライセンス アクション
Psychopharmacology_237_2125.pdf Psychopharmacology_237_2125.pdf (1.1 MB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル The role of glucocorticoid receptors in the induction and prevention of hippocampal abnormalities in an animal model of posttraumatic stress disorder
言語 en
作成者 Araki, Motoaki

× Araki, Motoaki

en Araki, Motoaki

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Fuchikami, Manabu

× Fuchikami, Manabu

en Fuchikami, Manabu

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Omura, Jun

× Omura, Jun

en Omura, Jun

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Miyagi, Tatsuhiro

× Miyagi, Tatsuhiro

en Miyagi, Tatsuhiro

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Nagashima, Nobuyuki

× Nagashima, Nobuyuki

en Nagashima, Nobuyuki

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Okamoto, Yasumasa

× Okamoto, Yasumasa

en Okamoto, Yasumasa

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Morinobu , Shigeru

× Morinobu , Shigeru

en Morinobu , Shigeru

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 This is a post-peer-review, pre-copyedit version of an article published in Psychopharmacology. The final authenticated version is available online at: https://doi.org/10.1007/s00213-020-05523-x
権利情報
権利情報 This is not the published version. Please cite only the published version. この論文は出版社版ではありません。引用の際には出版社版をご確認、ご利用ください。
主題
主題Scheme Other
主題 Animal model
主題
主題Scheme Other
主題 Posttraumatic stress disorder (PTSD)
主題
主題Scheme Other
主題 Glucocorticoid receptor (GR)
主題
主題Scheme Other
主題 GR antagonist
内容記述
内容記述 Rationale: Since the precise mechanisms of posttraumatic stress disorder (PTSD) remain unknown, effective treatment interventions have not yet been established. Numerous clinical studies have led to the hypothesis that elevated glucocorticoid levels in response to extreme stress might trigger a pathophysiological cascade which consequently leads to functional and morphological changes in the hippocampus. Objectives: To elucidate the pathophysiology of PTSD, we examined the alteration of hippocampal gene expression through the glucocorticoid receptor (GR) in the single prolonged stress (SPS) paradigm, a rat model of PTSD. Methods: We measured nuclear GRs by western blot, and the binding of GR to the promoter of Bcl-2 and Bax genes by chromatin immunoprecipitation-qPCR as well as the expression of these 2 genes by RT-PCR in the hippocampus of SPS rats. In addition, we examined the preventive effects of a GR antagonist on SPS-induced molecular, morphological, and behavioral alterations (hippocampal gene expression of Bcl-2 and Bax, hippocampal apoptosis using TUNEL staining, impaired fear memory extinction (FME) using the contextual fear conditioning paradigm). Results: Exposure to SPS increased nuclear GR expression and GR binding to Bcl-2 gene, and decreased Bcl-2 mRNA expression. Administration of GR antagonist immediately after SPS prevented activation of the glucocorticoid cascade, hippocampal apoptosis, and impairment FME in SPS rats. Conclusion: The activation of GRs in response to severe stress may trigger the pathophysiological cascade leading to impaired FME and hippocampal apoptosis. In contrast, administration of GR antagonist could be useful for preventing the development of PTSD.
言語 en
内容記述
内容記述タイプ Other
内容記述 This work was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI (a grant-in aid for Scientific Research, C) Grant Number JP18K07562, and Takeda Science Foundation.
出版者
出版者 Springer
言語
言語 eng
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 journal article
出版タイプ
出版タイプ AO
出版タイプResource http://purl.org/coar/version/c_b1a7d7d4d402bcce
関連情報
識別子タイプ DOI
関連識別子 10.1007/s00213-020-05523-x
関連情報
識別子タイプ PMID
関連識別子 32333135
関連情報
識別子タイプ DOI
関連識別子 https://doi.org/10.1007/s00213-020-05523-x
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0033-3158
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1432-2072
開始ページ
開始ページ 2125
書誌情報 Psychopharmacology
Psychopharmacology

巻 237, 号 7, p. 2125-2137, 発行日 2020-07
旧ID 50463
備考 Post-print version/PDF may be used in an institutional repository after an embargo period of 12 months.
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