Abstract
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.
Highlights
Stress is one major concern affecting mental health of general population, and leads to a series of cognitive disorders including memory deficits.[1]
Stress-induced anxiety behavior and spine loss in barrel cortex can be rescued by physical exercise We first tested whether treadmill exercise could ameliorate stressrelated behavior abnormality
The results showed no significant difference of spine formation among all groups (F (3,20) = 0.97, P40.05, one-way analysis of variance; Figure 1e)
Summary
Stress is one major concern affecting mental health of general population, and leads to a series of cognitive disorders including memory deficits.[1]. Dendritic spine dynamics including formation, elimination and retention have been studied regarding its correlation with memory function. Stress can induce dendritic spine loss in prefrontal cortex,[2] amygdala[3] and hippocampus.[4]. Such effects are likely to be caused by neurotrophic factors such as brain-derived nerve growth factor (BDNF).[5] The suppressed spinogenesis in hippocampus may further contribute to stressinduced memory deficit.[6] Our previous findings showed the improvement of hippocampal neurogenesis and depression-like behavior by physical exercise.[7] it is still unclear whether exercise has similar antidepressant effect in cortical regions
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