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首页> 外文期刊>Acta neurobiologiae experimentalis >Injury induced dendritic plasticity in the mature central nervous system.
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Injury induced dendritic plasticity in the mature central nervous system.

机译：损伤在成熟的中枢神经系统中引起树突状可塑性。

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摘要

Injury to the mature central nervous system (CNS) induces a series of transient changes leading not only to death of neurons, but also to spontaneous rearrangement of the affected network. One of such pro plastic events, detected following injury, is an increased level of neurotrophins. Neurotrophins are a family of proteins involved in survival and outgrowth processes. The other one, more difficult to observe, is a change in the complexity of the dendritic tree, causing arborization or pruning, depending on many circumstances: i.e. lesion etiology. Subsequent therapies like enriched environment or locomotor exercise bring about a functional improvement, which was found to further increase the neurotrophin level and induced additional arborization of dendrites. Another important consequence of damage to CNS connections is deafferentation, shown to induce a down regulation of outgrowth inhibitors. Their suppression in turn may facilitate dendritic plasticity. Taken together, these factors may contributeto enhanced plasticity in the injured mature CNS. Thus the proper use of endogenously increased plastic potential seems to be important for design and optimizing therapeutic strategies. Further investigation of mechanisms involved in switching on plasticity may help to improve on existing therapies and find new ways to obtain better recovery following injury.
机译：损伤成熟的中枢神经系统（CNS）会引起一系列瞬时变化，不仅导致神经元死亡，而且还导致受影响网络的自发重排。损伤后检测到的此类促塑事件是神经营养蛋白水平升高。神经营养蛋白是涉及生存和生长过程的蛋白质家族。另一个较难观察到的是树状树的复杂性发生变化，导致乔木化或修剪，这取决于许多情况：即病因。随后的疗法，如丰富的环境或运动锻炼，带来了功能上的改善，发现该疗法可进一步增加神经营养蛋白水平并诱导树突的进一步乔化。损害中枢神经系统连接的另一个重要结果是脱除咖啡因，这表明会导致抑制下调生长的作用。反过来抑制它们可以促进树突状可塑性。综上所述，这些因素可能有助于增强受损中枢神经系统的可塑性。因此，内源性增加的可塑性潜力的正确使用对于设计和优化治疗策略似乎很重要。对涉及可塑性的机制的进一步研究可能有助于改善现有疗法，并找到新的方法以在受伤后获得更好的康复。

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