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脑与脊髓的相互作用:损伤前运动对脊髓的保护作用。

Brain and spinal cord interaction: protective effects of exercise prior to spinal cord injury.

机构信息

Department of Integrative Biology and Physiology, University of California Los Angeles, Los Angeles, California, United States of America.

出版信息

PLoS One. 2012;7(2):e32298. doi: 10.1371/journal.pone.0032298. Epub 2012 Feb 22.

Abstract

We have investigated the effects of a spinal cord injury on the brain and spinal cord, and whether exercise provided before the injury could organize a protective reaction across the neuroaxis. Animals were exposed to 21 days of voluntary exercise, followed by a full spinal transection (T7-T9) and sacrificed two days later. Here we show that the effects of spinal cord injury go beyond the spinal cord itself and influence the molecular substrates of synaptic plasticity and learning in the brain. The injury reduced BDNF levels in the hippocampus in conjunction with the activated forms of p-synapsin I, p-CREB and p-CaMK II, while exercise prior to injury prevented these reductions. Similar effects of the injury were observed in the lumbar enlargement region of the spinal cord, where exercise prevented the reductions in BDNF, and p-CREB. Furthermore, the response of the hippocampus to the spinal lesion appeared to be coordinated to that of the spinal cord, as evidenced by corresponding injury-related changes in BDNF levels in the brain and spinal cord. These results provide an indication for the increased vulnerability of brain centers after spinal cord injury. These findings also imply that the level of chronic activity prior to a spinal cord injury could determine the level of sensory-motor and cognitive recovery following the injury. In particular, exercise prior to the injury onset appears to foster protective mechanisms in the brain and spinal cord.

摘要

我们研究了脊髓损伤对脑和脊髓的影响,以及损伤前的运动是否能在神经轴上组织起一种保护反应。动物接受 21 天的自愿运动,然后进行完全的脊髓横切(T7-T9),并在两天后处死。在这里,我们表明脊髓损伤的影响超出了脊髓本身,影响了大脑中突触可塑性和学习的分子基础。损伤降低了海马体中的 BDNF 水平,同时激活了 p-synapsin I、p-CREB 和 p-CaMK II 的形式,而损伤前的运动则阻止了这些降低。在脊髓的腰膨大区也观察到了类似的损伤效应,运动阻止了 BDNF 和 p-CREB 的减少。此外,海马体对脊髓损伤的反应似乎与脊髓的反应相协调,这可以从大脑和脊髓中 BDNF 水平的相应损伤相关变化得到证明。这些结果表明,脊髓损伤后大脑中枢的脆弱性增加。这些发现还表明,脊髓损伤前的慢性活动水平可能决定损伤后的感觉运动和认知恢复水平。特别是,损伤前的运动似乎促进了大脑和脊髓中的保护机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9cf8/3284558/085b905f845f/pone.0032298.g001.jpg

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