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首页> 外文期刊>Journal of neurotrauma >Delayed and Abbreviated Environmental Enrichment after Brain Trauma Promotes Motor and Cognitive Recovery That Is Not Contingent on Increased Neurogenesis
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Delayed and Abbreviated Environmental Enrichment after Brain Trauma Promotes Motor and Cognitive Recovery That Is Not Contingent on Increased Neurogenesis

机译：脑创伤后的延迟和缩写的环境富集促进了不存在于神经发生的增加的运动和认知恢复

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Environmental enrichment (EE) confers motor and cognitive recovery in pre-clinical models of traumatic brain injury (TBI), and neurogenesis has been attributed to mediating the benefits. Whether that ascription is correct has not been fully investigated. Hence, the goal of the current study is to further clarify the possible role of learning-induced hippocampal neurogenesis on functional recovery after cortical impact or sham injury by utilizing two EE paradigms (i.e., early + continuous, initiated immediately after TBI and presented 24h/day; and delayed + abbreviated, initiated 4 days after TBI for 6h/day) and comparing them to one another as well as to standard (STD) housed controls. Motor and cognitive performance was assessed on post-operative Days 1-5 and 14-19, respectively, for the STD and early + continuous EE groups and on Days 4-8 and 17-22, for the delayed + abbreviated EE groups. Rats were injected with bromodeoxyuridine (BrdU, 500mg/ kg; intraperitoneally) for 3 days (12h apart) before cognitive training and sacrificed 1 week later for quantification of BrdU+ and doublecortin (DCX+) labeled cells. Both early + continuous and delayed + abbreviated EE promoted motor and cognitive recovery after TBI, relative to STD (p 0.05). However, only early + continuous EE increased DCX+ cells beyond the level of STD-housed controls (p<0.05). No effect of EE on non-injured controls was observed. Based on these data, two novel conclusions emerged. First, EE does not need to be provided early and continuously after TBI to confer benefits, which lends credence to the delayed + abbreviated EE paradigm as a relevant pre-clinical model of neurorehabilitation. Second, the functional recovery observed after TBI in the delayed + abbreviated EE paradigm is not contingent on increased hippocampal neurogenesis. Future studies will elucidate alternate viable mechanisms mediating the benefits induced by EE.
机译：环境富集（EE）在创伤性脑损伤（TBI）前临床前模型中的电动机和认知恢复，神经发生归因于调解这些益处。归属是否正确尚未得到完全调查。因此，目前研究的目的是通过利用两个EE范例（即，在TBI之后立即启动并呈现24h /呈现24h /日;和延迟+缩写，在TBI后4天开始6小时/天）并将其彼此与标准（STD）进行比较。在术后第1-5和14-19次对STD和早期+连续EE组和第4-8和17-22组分别评估电动机和认知性能，用于延迟+缩写EE组。在认知训练之前用溴酰氧基尿苷（Brdu，500mg / kg;腹膜内）注射大鼠3天（12h分开），并在1周后处死1周，以定量Brdu +和双峰（DCx +）标记细胞。早期+连续和延迟+缩写EE促进TBI后的电动机和认知恢复，相对于STD（P 0.05）。然而，只有早期+连续EE增加DCX +细胞，超过STD容纳的对照水平（P <0.05）。观察到EE对非损伤对照的影响。基于这些数据，出现了两种新的结论。首先，在TBI之后不需要在TBI授予福利之后提前和连续提供，这将抵消延迟+缩写EE范例作为神经孢子率的相关临床模型。其次，在延迟+缩写EE范例中观察到在TBI中观察到的功能恢复不存在于增加的海马神经发生增加。未来的研究将阐明介导EE诱导的益处的替代可行机制。

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