The role of circadian clock gene Arntl in the winter depression-like behavior in melatonin-proficient female CBA/N mice.

Circadian rhythm Melatonin Photoperiodic response Winter depression

Journal

Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516

Informations de publication

Date de publication:
02 Oct 2024
Historique:
received: 27 09 2024
accepted: 01 10 2024
medline: 7 10 2024
pubmed: 7 10 2024
entrez: 6 10 2024
Statut: aheadofprint

Résumé

Seasonal affective disorder (SAD), also known as winter depression, is a subtype of depression typically manifesting in winter. Typical symptoms of SAD, such as an increased need for sleep and carbohydrate cravings associated with increased appetite and weight, are distinct from those of major depression, and the underlying mechanisms of SAD remain unclear. Although laboratory mice are generally considered non-seasonal animals, we observed depression-like behaviors in melatonin-proficient female CBA/N mice maintained under winter-mimicking conditions. Transcriptome analysis of the brains of CBA/N mice maintained under winter- and summer-mimicking conditions revealed changes in the expression of circadian clock genes, including Arntl (also known as Bmal1). We generated Arntl-deficient, melatonin-proficient CBA/N mice using the speed congenic method to examine the role of Arntl in depressive behavior. The tail suspension test in these mice revealed a depressive phenotype. These results suggested that the circadian clock gene Arntl may be involved in winter depression-like behavior.

Identifiants

pubmed: 39369541
pii: S0006-291X(24)01326-3
doi: 10.1016/j.bbrc.2024.150790
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

150790

Informations de copyright

Copyright © 2024 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest Authors declare that they have no competing interests.

Auteurs

Liang Ren (L)

Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, 464-8601, Japan; Laboratory of Animal Integrative Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601, Japan.

Kousuke Okimura (K)

Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, 464-8601, Japan; Laboratory of Animal Integrative Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601, Japan.

Akira Ishikawa (A)

Laboratory of Animal Genetics and Breeding, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601, Japan.

Naohiro Kon (N)

Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, 464-8601, Japan; Laboratory of Animal Integrative Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601, Japan.

Shigeki Shimba (S)

Department of Health Science, School of Pharmacy, Nihon University, 7-7-1 Narashinodai, Funabashi, Chiba, 274-8555, Japan.

Takashi Yoshimura (T)

Institute of Transformative Bio-Molecules (WPI-ITbM), Nagoya University, Nagoya, 464-8601, Japan; Laboratory of Animal Integrative Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601, Japan; Center for One Medicine Innovative Translational Research (COMIT), Nagoya University, Nagoya, 464-8601, Japan. Electronic address: takashiy@agr.nagoya-u.ac.jp.

Classifications MeSH