Comparative analysis of restraint stress-induced depressive-like phenotypes in C57BL/6N mice derived from three different sources

C57BL/6NKorl mice are a novel mouse stock recently developed by the National Institute of Food and Drug Safety Evaluation in Korea. Extensive research into the nature of C57BL/6NKorl mice is being conducted. However, there is no scientific evidence for the phenotypic response to restraint stress (RS...

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Published inLaboratory animal research Vol. 36; no. 1; pp. 1 - 9
Main Authors Hwang, Dong-Joo, Kwon, Ki-Chun, Hwang, Dae-Youn, Seo, Min-Soo, Kim, Kil-Soo, Jung, Young-Suk, Cho, Joon-Yong
Format Journal Article
LanguageEnglish
Published Seole BioMed Central 26.08.2020
BMC
한국실험동물학회
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Summary:C57BL/6NKorl mice are a novel mouse stock recently developed by the National Institute of Food and Drug Safety Evaluation in Korea. Extensive research into the nature of C57BL/6NKorl mice is being conducted. However, there is no scientific evidence for the phenotypic response to restraint stress (RST), a stress paradigm for modeling depressive disorders, in rodents. In this study, we investigated the repeated RST-induced depressive-like phenotypes in C57BL/6 N mouse substrains (viz., C57BL/6NKorl mice from Korea, C57BL/6NA mice from the United States, and C57BL/6NB mice from Japan) obtained from different sources. The results showed that C57BL/6 N mice derived from various sources exposed to repeated RST resulted in depressive-like phenotypes reflected by a similar degree of behavioral modification and susceptibility to oxidative stress in a duration-dependent manner, except for the distinctive features (increased body weight (BW) and tolerance to the suppression of BW gain by exposure to repeated RST) in C57BL/6NKorl mice. Taken together, the duration-dependent alteration in depressive-like phenotypes by repeated exposure to RST observed in this study may provide valuable insights into the nature of C57BL/6NKorl mice as an alternative animal resource for better understanding of the etiology of depressive disorders and the mechanisms of antidepressant actions.
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ISSN:2233-7660
1738-6055
2233-7660
DOI:10.1186/s42826-020-00062-0