Rapid and long-lasting antidepressant-like effects of the pituitary adenylate cyclase-activating polypeptide receptor antagonist PA-915 in chronic stress mouse models
Stress-related disorders, such as depression and anxiety, have been one of the most important medical issues. Accumulating evidence suggests that the activation of the pituitary adenylate cyclase-activating polypeptide and its receptor PAC1 are involved in the stress axis and the development of stress-related disorders. We recently developed PA-915, a small-molecule, non-peptide, high-affinity PAC1 antagonist, and demonstrated that it significantly suppresses anxiety-like behavior in acute stress-induced mice. In this study, we aimed to investigate the behavioral effects of PA-915 in chronic stress-induced mouse models of depression, which included repeated social defeat stress, repeated corticosterone administration, and social isolation rearing. PA-915 ameliorated the increased immobility time in the forced swim test in these stress-induced mice. In repeated social defeat stress mice, PA-915 improved anxiety-like and depression-like behaviors and cognitive dysfunction, as assessed by the light-dark, open field, elevated plus maze, sucrose preference, forced swim, Y-maze, and novel object recognition tests. In addition, we evaluated the usefulness of PA-915 as an antidepressant and compared it with ketamine and fluoxetine. In the sucrose preference test, an antidepressant-like effect was observed for 8 weeks in mice that received a single dose of PA-915, which was a similar effect observed with ketamine. In non-stressed control mice, PA-915 did not induce behavioral abnormalities, such as hyperlocomotion, cognitive dysfunction, or dependency. The present results show that PA-915 improves anxiety-like behaviors and cognitive impairment and exerts rapid and long-lasting antidepressant effects in chronic stress-induced mouse models of anxiety and depression, proposing a promising treatment option for stress-related disorders.
Authors
- Toru Takumi (ORCID: https://orcid.org/0000-0001-7153-266X)
- Kazuto Nunomura (ORCID: https://orcid.org/0000-0002-6444-3244)
- Yukio Ago
- Naoki Toyooka (ORCID: https://orcid.org/0000-0002-9568-1528)
- Atsuro Miyata (ORCID: https://orcid.org/0000-0003-3959-331X)
- Kazuhiro Takuma (ORCID: https://orcid.org/0000-0001-6484-1122)
- Hitoshi Hashimoto (ORCID: https://orcid.org/0000-0001-6548-4016)
- Takashi Kurihara (ORCID: https://orcid.org/0000-0003-4001-6771)
- Ichiro Takasaki (ORCID: https://orcid.org/0000-0002-6083-1119)
- Tetsuya Oguri (ORCID: https://orcid.org/0000-0002-3796-7915)
- Takuya Okada (ORCID: https://orcid.org/0000-0003-2228-7711)
- Atsuko Hayata‐Takano (ORCID: https://orcid.org/0000-0002-4992-2845)
- Rei Takeshita
- Kenichiro Murata
- Yui Yamano
- Bangzhong Lin (ORCID: https://orcid.org/0000-0001-5877-949X)
- Manato Ikuta
- Yusuke Shintani (ORCID: https://orcid.org/0000-0002-5488-2761)
- Shinsaku Nakagawa
- Chiaki Asaka
Institutions
- Kagoshima University (JP)
- Hiroshima University (JP)
- University of Toyama (JP)
- Kobe University (JP)
- The University of Osaka (JP)
Publication Details
- Journal
- Molecular Psychiatry
- Published
- 2025-09-04
- DOI
- https://doi.org/10.1038/s41380-025-03209-4
- Citations
- 1
- Primary Topic
- Stress Responses and Cortisol
- Type
- article
- Field-Weighted Citation Impact
- 1.11
Funders
- Takeda Science Foundation
- Nakatomi Foundation
- Japan Agency for Medical Research and Development
- Ministry of Education, Culture, Sports, Science and Technology
- Nakatani Foundation for Advancement of Measuring Technologies in Biomedical Engineering
- Japan Society for the Promotion of Science