Exercise, but not environmental enrichment, improves learning after kainic acid-induced hippocampal neurodegeneration in association with an increase in brain-neurotrophic factor

Exercise, but not environmental enrichment, improves learning after kainic acid-induced hippocampal neurodegeneration in association with an increase in brain-neurotrophic factor
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DOI:
10.1016/j.bbr.2004.09.021
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发表时间:
2005-04-15
影响因子:
2.7
通讯作者:
O'Mara, SM
O'Mara, SM
中科院分区:
心理学3区
文献类型:
--
作者:
Gobbo, OL;O'Mara, SM

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以前的研究表明,在跑步轮上运动可以保护神经,这可能是由于运动后基因表达的变化,营养蛋白的增加和/或心血管反应性的增强。在这里,我们要问的是,体育锻炼或丰富的环境是否能在脑损伤后提供保护,特别是在认知功能的恢复方面。为了评估这些条件的神经保护作用,我们使用红藻氨酸(KA)模型的神经元损伤。系统性乙酰胆碱酯酶KA通过过度刺激谷氨酸受体诱导兴奋性毒性,导致神经元坏死和凋亡死亡。我们的研究结果表明,运动,而不是丰富的环境,KA诱导的脑损伤之前,改善行为表现在Morris水迷宫和对象探索任务。然而.先前的运动没有将KA处理的动物中通常观察到的活动过度降低到对照水平,如通过在开放视野中的Amplitude测量的。此外,运动和丰富的环境都不能防止CA 1神经元的丢失。海马的CA 2和CA 3区。尽管运动和KA处理的动物的齿状回中脑源性神经营养因子(BDNF)水平显著增加。(c)2004年由Elsevier B. V.出版
Previous studies have suggested that exercise in a running wheel can be neuroprotective, perhaps due to, among others, gene-expression changes after exercise, increases in trophic proteins and/or enhanced cardiovascular responsivity. Here we ask whether physical exercise or environmental enrichment provide protection after brain damage, especially in terms of recovery of cognitive function. To evaluate the neuroprotective effect of these conditions, we used the kainic acid (KA) model of neuronal injury. Systernically-achninistered KA induces excitotoxicity by overstimulation of glutamate receptors, resulting in neuronal death by necrosis and apoptosis. Our results show that exercise, but not enriched environment, prior to KA-induced brain damage, improved behavioural performance in both Morris watermaze and object exploration tasks. However. prior exercise did not decrease to control levels the hyperactivity normally seen in KA-treated animals, as measured by ambulation in the open field. Furthermore, both exercise and enriched environment did not protect against neuron loss in CA1. CA2 and CA3 areas of the hippocampus. despite a substantial increase in brain-derived neutrophic factor (BDNF) levels in dentate gyrus of the exercise and KA-treated animals. (c) 2004 Published by Elsevier B.V.