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首页> 外文期刊>The European Journal of Neuroscience >Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition.
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Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition.

机译：海马BDNF介导运动对突触可塑性和认知的功效。

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Abstract We found that a short exercise period enhanced cognitive function on the Morris water maze (MWM), such that exercised animals were significantly better than sedentary controls at learning and recalling the location of the platform. The finding that exercise increased brain-derived neurotrophic factor (BDNF), a molecule important for synaptic plasticity and learning and memory, impelled us to examine whether a BDNF-mediated mechanism subserves the capacity of exercise to improve hippocampal-dependent learning. A specific immunoadhesin chimera (TrkB-IgG), that mimics the BDNF receptor, TrkB, to selectively bind BDNF molecules, was used to block BDNF in the hippocampus during a 1-week voluntary exercise period. After this, a 2-trial-per-day MWM was performed for 5 consecutive days, succeeded by a probe trial 2 days later. By inhibiting BDNF action we blocked the benefit of exercise on cognitive function, such that the learning and recall abilities of exercising animals receiving the BDNF blocker were reduced to sedentary control levels. Inhibiting BDNF action also blocked the effect of exercise on downstream systems regulated by BDNF and important for synaptic plasticity, cAMP response-element-binding protein (CREB) and synapsin I. Specific to exercise, we found an association between CREB and BDNF expression and cognitive function, such that animals who were the fastest learners and had the best recall showed the highest expression of BDNF and associated CREB mRNA levels. These findings suggest a functional role for CREB under the control of BDNF in mediating the exercise-induced enhancement in learning and memory. Our results indicate that synapsin I might also contribute to this BDNF-mediated mechanism.
机译：摘要我们发现，短时间运动会增强莫里斯水迷宫（MWM）的认知功能，因此运动的动物在学习和记忆平台的位置上明显优于久坐的对照组。锻炼增加了脑源性神经营养因子（BDNF）的发现，BDNF是一种对突触可塑性和学习记忆具有重要作用的分子，促使我们研究BDNF介导的机制是否有助于锻炼改善海马依赖型学习的能力。模仿BDNF受体TrkB选择性结合BDNF分子的特异性免疫粘附素嵌合体（TrkB-IgG）在1周的自愿运动期间被用来阻断海马中的BDNF。此后，连续2天每天进行2次MWM试验，然后2天后进行了探针试验。通过抑制BDNF的作用，我们阻止了运动对认知功能的好处，从而使接受BDNF阻断剂的运动动物的学习和记忆能力降低到了久坐控制水平。抑制BDNF的作用还阻断了运动对受BDNF调节的下游系统的影响，该系统对于突触可塑性，cAMP反应元件结合蛋白（CREB）和突触蛋白I很重要。特定于运动，我们发现CREB和BDNF的表达与认知之间存在关联因此，学习速度最快，召回率最高的动物表现出最高的BDNF表达水平和相关的CREB ​​mRNA水平。这些发现表明，CREB在BDNF的控制下在介导运动诱导的学习和记忆增强中发挥了功能性作用。我们的结果表明，突触蛋白I可能也参与了BDNF介导的机制。

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