JaLCDOI |
10.18926/AMO/60368
|
フルテキストURL |
74_4_301.pdf
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著者 |
Takahashi, Kei|
Kitamura, Yoshihisa|
Ushio, Soichiro|
Sendo, Toshiaki|
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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
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Amo Type |
Original Article
|
出版物タイトル |
Acta Medica Okayama
|
発行日 |
2020-08
|
巻 |
74巻
|
号 |
4号
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出版者 |
Okayama University Medical School
|
開始ページ |
301
|
終了ページ |
306
|
ISSN |
0386-300X
|
NCID |
AA00508441
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資料タイプ |
学術雑誌論文
|
言語 |
英語
|
著作権者 |
CopyrightⒸ 2020 by Okayama University Medical School
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論文のバージョン |
publisher
|
査読 |
有り
|
PubMed ID |
32843761
|
Web of Science KeyUT |
000562508700005
|
NAID |
120006880207
|