Voluntary exercise following traumatic brain injury: Brain-derived neurotrophic factor upregulation and recovery of function
Voluntary exercise following traumatic brain injury: Brain-derived neurotrophic factor upregulation and recovery of function
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DOI：
10.1016/j.neuroscience.2004.01.030
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发表时间：
2004-01-01
期刊：
影响因子：
3.3
通讯作者：
Gomez-Pinilla, F
中科院分区：
文献类型：
--
作者：
Griesbach, GS;Hovda, DA;Gomez-Pinilla, F
随意运动导致脑源性神经营养因子（BDNF）和参与突触功能的相关蛋白质的上调。活动诱导的神经可塑性增强可被考虑用于创伤性脑损伤（TBI）的治疗。考虑到在伤后第一周内，大脑正在经历动态恢复过程和可能影响运动结果的能量变化，我们评估了实验性TBI后急性和延迟运动的影响。雄性Sprague-Dawley大鼠接受假手术或侧向液压冲击损伤（FPI），并在损伤后0-6天（急性）或14-20天（延迟）在有或没有转轮（RW）的情况下圈养。FPI单独导致损伤后第7天海马磷酸化突触蛋白I和磷酸化环AMP反应元件结合蛋白（CREB）水平显著升高，其中磷酸化CREB在损伤后第21天仍然升高。假手术和延迟FPI-RW大鼠运动后BDNF水平升高。运动也增加磷酸化突触蛋白I和CREB在假手术大鼠。与假手术组相比，急性运动FPI大鼠没有表现出活动依赖性BDNF上调，磷酸化突触蛋白I和总CREB显著减少。在急性或延迟RW暴露后，通过利用Morris水迷宫评估其他大鼠的认知（学习获得和记忆）。假手术和延迟FPI-RW动物从运动中受益，与延迟FPI-久坐大鼠相比，达到标准的试验次数显著减少（连续四次试验在7秒或更短时间内定位平台的能力）。相反，与所有其他组相比，急性FPI-RW大鼠的认知能力显著受损。这些结果表明，自愿运动可以内源性上调BDNF，并促进TBI后延迟恢复。然而，当TBI后不久进行运动时，对运动的分子反应被破坏，恢复可能会延迟。(C)2004年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Voluntary exercise leads to an upregulation of brain-derived neurotrophic factor (BDNF) and associated proteins involved in synaptic function. Activity-induced enhancement of neuroplasticity may be considered for the treatment of traumatic brain injury (TBI). Given that during the first postinjury week the brain is undergoing dynamic restorative processes and energetic changes that may influence the outcome of exercise, we evaluated the effects of acute and delayed exercise following experimental TBI. Male Sprague-Dawley rats underwent either sham or lateral fluid-percussion injury (FPI) and were housed with or without access to a running wheel (RW) from postinjury days 0-6 (acute) or 14-20 (delayed). FPI alone resulted in significantly elevated levels of hippocampal phosphorylated synapsin I and phosphorylated cyclic AMP response element-binding-protein (CREB) at postinjury day 7, of which phosphorylated CREB remained elevated at postinjury day 21. Sham and delayed FPI-RW rats showed increased levels of BDNF, following exercise. Exercise also increased phosphorylated synapsin I and CREB in sham rats. In contrast to shams, the acutely exercised FPI rats failed to show activity-dependent BDNF upregulation and had significant decreases of phosphorylated synapsin I and total CREB. Additional rats were cognitively assessed (learning acquisition and memory) by utilizing the Morris water maze after acute or delayed RW exposure. Shams and delayed FPI-RW animals benefited from exercise, as indicated by a significant decrease in the number of trials to criterion (ability to locate the platform in 7 s or less for four consecutive trials), compared with the delayed FPI-sedentary rats. In contrast, cognitive performance in the acute FPI-RW rats was significantly impaired compared with all the other groups. These results suggest that voluntary exercise can endogenously upregulate BDNF and enhance recovery when it is delayed after TBI. However, when exercise is administered to soon after TBI, the molecular response to exercise is disrupted and recovery may be delayed. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.