Modulation of adult-born neurons in the inflamed hippocampus.

Modulation of adult-born neurons in the inflamed hippocampus.
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DOI:
10.3389/fncel.2013.00145
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发表时间:
2013-09-06
影响因子:
5.3
通讯作者:
Rosi S
Rosi S
中科院分区:
医学2区
文献类型:
--
作者:
Belarbi K;Rosi S

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在人的一生中,新的神经元不断地被添加到与空间学习和记忆有关的海马回路中。这些新细胞起源于齿状回颗粒下区的神经前体,迁移到颗粒细胞层,并整合到编码空间和上下文信息的神经网络中。这一过程可能受到几种环境和内源性因素的影响,并在不同的神经系统疾病动物模型中得到改变。由活化的小胶质细胞的存在所定义的神经炎症是神经系统疾病进展的常见关键因素。对文献的分析表明,小胶质细胞活化不仅影响新神经元的产生,而且影响新神经元的迁移和募集。小胶质细胞对成人出生的神经元的影响似乎比以往任何时候都设想的多得多,结合了依赖于激活表型和释放的因子的支持和有害作用。因此,旨在将小胶质细胞改变为促进功能性神经发生的状态的策略的发展可以为与认知缺陷和神经炎症相关的神经系统疾病提供新的治疗机会。本综述总结了目前的知识,如何生产,分布和招聘新的神经元到行为相关的神经网络被修改在发炎的海马。
Throughout life new neurons are continuously added to the hippocampal circuitry involved with spatial learning and memory. These new cells originate from neural precursors in the subgranular zone of the dentate gyrus, migrate into the granule cell layer, and integrate into neural networks encoding spatial and contextual information. This process can be influenced by several environmental and endogenous factors and is modified in different animal models of neurological disorders. Neuroinflammation, as defined by the presence of activated microglia, is a common key factor to the progression of neurological disorders. Analysis of the literature shows that microglial activation impacts not only the production, but also the migration and the recruitment of new neurons. The impact of microglia on adult-born neurons appears much more multifaceted than ever envisioned before, combining both supportive and detrimental effects that are dependent upon the activation phenotype and the factors being released. The development of strategies aimed to change microglia toward states that promote functional neurogenesis could therefore offer novel therapeutic opportunities against neurological disorders associated with cognitive deficits and neuroinflammation. The present review summarizes the current knowledge on how production, distribution, and recruitment of new neurons into behaviorally relevant neural networks are modified in the inflamed hippocampus.
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