Immobility-reducing effects of ketamine during the forced swim test on 5-HT1A receptor activity in the medial prefrontal cortex in an intractable depression model

Kei Takahashi, Yoshihisa Kitamura, Soichiro Ushio, Toshiaki Sendo

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)301-306
Number of pages6
JournalActa medica Okayama
Volume74
Issue number4
Publication statusPublished - 2020

Keywords

  • 5-HT receptor
  • Adrenocorticotropic hormone
  • Forced swim test
  • Ketamine
  • Medial prefrontal cortex

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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