JaLCDOI 10.18926/AMO/60368
フルテキストURL 74_4_301.pdf
著者 Takahashi, Kei| Kitamura, Yoshihisa| Ushio, Soichiro| Sendo, Toshiaki|
抄録 Ketamine has been clinically proven to ameliorate depression, including treatment-resistant depression. The detailed mechanism of action of ketamine in treatment-resistant depression remains unclear. We examined the effects of ketamine on the immobility times of adrenocorticotropic hormone (ACTH)-treated rats during the forced swim test, and we explored the mechanism by which ketamine acts in this model. We investigated the neuroanatomical site of action by microinjecting ketamine into the medial prefrontal cortex of rats. A significant reduction of the rats’ immobility during the forced swim test was observed after the intraperitoneal injection of ketamine in both saline- and ACTH-treated rats. The microinjection of ketamine into the medial prefrontal cortex also decreased immobility during the forced swim test in both saline- and ACTH-treated rats. The immobility-decreasing effect of intraperitoneally injected ketamine was blocked by administering WAY100635, a 5-HT1A receptor antagonist, into the medial prefrontal cortex. These findings contribute to the evidence that ketamine can be useful against treatment-resistant depressive conditions. The immobility-reducing effects of ketamine might be mediated by 5-HT1A receptor activity in the medial prefrontal cortex.
キーワード ketamine adrenocorticotropic hormone forced swim test medial prefrontal cortex 5-HT1A receptor
Amo Type Original Article
発行日 2020-08
出版物タイトル Acta Medica Okayama
出版者 Okayama University Medical School
開始ページ 301
終了ページ 306
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2020 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 32843761
Web of Science KeyUT 000562508700005
NAID 120006880207
著者 高橋 圭|
発行日 2009-03-25
資料タイプ 学位論文