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

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作者
Dong-Joo Hwang
Ki-Chun Kwon
Dae-Youn Hwang
Min-Soo Seo
Kil-Soo Kim
Young-Suk Jung
Joon-Yong Cho
机构
[1] Korea National Sport University,Exercise Biochemistry Laboratory
[2] Pusan National University,Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute
[3] Daegu-Gyeongbuk Medical Innovation Foundation,Laboratory Animal Center
[4] Kyungpook National University,College of Veterinary Medicine
[5] Pusan National University,College of Pharmacy
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C57BL/6NKorl mice; Depressive disorder; Restraint stress;
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摘要
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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