Treadmill exercise suppressed stress-induced dendritic spine elimination in mouse barrel cortex and improved working memory via BDNF/TrkB pathway

被引:0
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作者
K Chen
L Zhang
M Tan
C S W Lai
A Li
C Ren
K-F So
机构
[1] Guangdong-Hong Kong-Macau Institute of CNS Regeneration,Department of Ophthalmology and State Key Laboratory of Brain and Cognitive Sciences
[2] Jinan University,undefined
[3] Guangdong Medical Key Laboratory of Brain Function and Diseases,undefined
[4] Jinan University,undefined
[5] Guangdong-Hong Kong-Macau Collaboration and Innovation Center for Tissue Regeneration and Repair,undefined
[6] Jinan University,undefined
[7] Co-Innovation Center of Neuroregeneration,undefined
[8] Nantong University,undefined
[9] School of Biomedical Sciences,undefined
[10] The University of Hong Kong,undefined
[11] The University of Hong Kong,undefined
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摘要
Stress-related memory deficit is correlated with dendritic spine loss. Physical exercise improves memory function and promotes spinogenesis. However, no studies have been performed to directly observe exercise-related effects on spine dynamics, in association with memory function. This study utilized transcranial two-photon in vivo microscopy to investigate dendritic spine formation and elimination in barrel cortex of mice under physical constrain or naive conditions, followed by memory performance in a whisker-dependent novel texture discrimination task. We found that stressed mice had elevated spine elimination rate in mouse barrel cortex plus deficits in memory retrieval, both of which can be rescued by chronic exercise on treadmill. Exercise also elevated brain-derived neurotrophic factor (BDNF) expression in barrel cortex. The above-mentioned rescuing effects for both spinognesis and memory function were abolished after inhibiting BDNF/tyrosine kinase B (TrkB) pathway. In summary, this study demonstrated the improvement of stress-associated memory function by exercise via facilitating spine retention in a BDNF/TrkB-dependent manner.
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页码:e1069 / e1069
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