Potential Involvement of Adiponectin Signaling in Regulating Physical Exercise-Elicited Hippocampal Neurogenesis and Dendritic Morphology in Stressed Mice

Frontiers in Cellular Neuroscience

Kwok-Fai So¹  Kenneth King-Yip Cheng²  Suk-Yu Yau⁶  Pingjie Wang⁷  Xin Sun⁷  Yiyao Liang⁷  Kai Chen⁷  Ang Li⁸  Aimin Xu^1,10 

[1] 0Co-innovation Center of Neuroregeneration, Nantong University, Nantong, China;Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong;Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong;Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong;Department of Pharmacy and Pharmacology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong;Department of Rehabilitation Sciences, The Hong Kong Polytechnic University, Kowloon, Hong Kong;Guangdong-Hong Kong-Macau Institute of CNS Regeneration, Joint International Research Laboratory of CNS Regeneration Ministry of Education, Jinan University, Guangzhou, China;Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China;State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong;State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Pokfulam, Hong Kong;

关键词: depression;    voluntary exercise;    adiponectin;    dentate gyrus;    hippocampal neurogenesis;    dendritic plasticity;   

DOI  :  10.3389/fncel.2020.00189

来源: DOAJ

【 摘 要 】

Adiponectin, a cytokine secreted by mature adipocytes, proves to be neuroprotective. We have previously reported that running triggers adiponectin up-regulation which subsequently promotes generation of hippocampal neurons and thereby alleviates depression-like behaviors in non-stressed mice. However, under the stressing condition, whether adiponectin could still exert antidepressant-like effects following exercise remained unexplored. In this study, by means of repeated corticosterone injections to mimic stress insult and voluntary wheel running as physical exercise intervention, we examined whether exercise-elicited antidepressive effects might involve adiponectin’s regulation on hippocampal neurogenesis and dendritic plasticity in stressed mice. Here we show that repeated injections of corticosterone inhibited hippocampal neurogenesis and impaired dendritic morphology of neurons in the dentate gyrus of both wild-type and adiponectin-knockout mice comparably, which subsequently evoked depression-like behaviors. Voluntary wheel running attenuated corticosterone-suppressed neurogenesis and enhanced dendritic plasticity in the hippocampus, ultimately reducing depression-like behaviors in wild-type, but not adiponectin-knockout mice. We further demonstrate that such proneurogenic effects were potentially achieved through activation of the AMP-dependent kinase (AMPK) pathway. Our study provides the first evidence that adiponectin signaling is essential for physical exercise-triggered effects on stress-elicited depression by retaining the normal proliferation of neural progenitors and dendritic morphology of neurons in the hippocampal dentate gyrus, which may depend on activation of the AMPK pathway.

【 授权许可】

Unknown