Indirect exposure to socially defeated conspecifics using recorded video activates the HPA axis and reduces reward sensitivity in mice.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
09 10 2020
Historique:
received: 29 05 2020
accepted: 24 09 2020
entrez: 10 10 2020
pubmed: 11 10 2020
medline: 9 3 2021
Statut: epublish

Résumé

Rodents perceive the emotional states of conspecifics using vision. In the present study, we demonstrated that exposure to the video-recorded distress of conspecifics induces stress responses in male C57BL/6J mice. A single exposure to a video-recorded scene of the social defeat stress (SDS) increased plasma corticosterone levels in these mice. This physiological change was suppressed by blocking the visual information, suggesting that vision plays a crucial role in inducing stress responses. Furthermore, after exposure to the video, there were increased numbers of c-Fos-positive neurons in the anterior cingulate cortex and other brain areas that are associated with the negative valence and empathy systems, but not in the regions related to the pain signaling. In addition, repeated exposure to SDS videos induced an apparent reduction in reward sensitivity in the sucrose preference test, but did not affect avoidance behaviour in the social interaction test or immobility behaviour in the forced swim test. Reduced reward sensitivity in mice reflects anhedonia, which is a core symptom of depression in humans. Our video SDS model therefore provides a unique opportunity to not only understand the mechanisms underlying stress-induced anhedonia, but also to screen effective candidate molecules for stress-related disorders with greater reproducibility.

Identifiants

pubmed: 33037312
doi: 10.1038/s41598-020-73988-z
pii: 10.1038/s41598-020-73988-z
pmc: PMC7547068
doi:

Substances chimiques

Proto-Oncogene Proteins c-fos 0
Corticosterone W980KJ009P

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

16881

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Auteurs

Yuko Nakatake (Y)

Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo, 187-8553, Japan.
Laboratory of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641, Yamazaki, Noda, Chiba, 278-8510, Japan.

Hiroki Furuie (H)

Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo, 187-8553, Japan.

Masatoshi Ukezono (M)

Developmental Disorder Data Multi-Level Integration Unit Medical Science Innovation Hub Program, RIKEN, 4-1-1 Kizugawadai, Kizugawa, Kyoto, 619-0225, Japan.

Misa Yamada (M)

Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo, 187-8553, Japan.

Kazumi Yoshizawa (K)

Laboratory of Pharmacology and Therapeutics, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641, Yamazaki, Noda, Chiba, 278-8510, Japan.

Mitsuhiko Yamada (M)

Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashimachi, Kodaira, Tokyo, 187-8553, Japan. mitsuhiko_yamada@ncnp.go.jp.

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