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Spinal Cord Injury Leads to Hippocampal Glial Alterations and Neural Stem Cell Inactivation
Cellular and Molecular Neurobiology ( IF 4 ) Pub Date : 2020-06-14 , DOI: 10.1007/s10571-020-00900-8
Ignacio Jure 1 , Alejandro F De Nicola 1, 2 , Juan Manuel Encinas 3 , Florencia Labombarda 1, 2
Affiliation  

The hippocampus encodes spatial and contextual information involved in memory and learning. The incorporation of new neurons into hippocampal networks increases neuroplasticity and enhances hippocampal-dependent learning performances. Only few studies have described hippocampal abnormalities after spinal cord injury (SCI) although cognitive deficits related to hippocampal function have been reported in rodents and even humans. The aim of this study was to characterize in further detail hippocampal changes in the acute and chronic SCI. Our data suggested that neurogenesis reduction in the acute phase after SCI could be due to enhanced death of amplifying neural progenitors (ANPs). In addition, astrocytes became reactive and microglial cells increased their number in almost all hippocampal regions studied. Glial changes resulted in a non-inflammatory response as the mRNAs of the major pro-inflammatory cytokines (IL-1β, TNFα, IL-18) remained unaltered, but CD200R mRNA levels were downregulated. Long-term after SCI, astrocytes remained reactive but on the other hand, microglial cell density decreased. Also, glial cells induced a neuroinflammatory environment with the upregulation of IL-1β, TNFα and IL-18 mRNA expression and the decrease of CD200R mRNA. Neurogenesis reduction may be ascribed at later time points to inactivation of neural stem cells (NSCs) and inhibition of ANP proliferation. The number of granular cells and CA1 pyramidal neurons decreased only in the chronic phase. The release of pro-inflammatory cytokines at the chronic phase might involve neurogenesis reduction and neurodegeneration of hippocampal neurons. Therefore, SCI led to hippocampal changes that could be implicated in cognitive deficits observed in rodents and humans.



中文翻译:

脊髓损伤导致海马胶质细胞改变和神经干细胞失活

海马体编码涉及记忆和学习的空间和上下文信息。将新神经元纳入海马网络可增加神经可塑性并增强海马依赖的学习表现。尽管在啮齿动物甚至人类中报告了与海马功能相关的认知缺陷,但只有少数研究描述了脊髓损伤 (SCI) 后的海马异常。本研究的目的是更详细地描述急性和慢性 SCI 的海马变化。我们的数据表明,脊髓损伤后急性期的神经发生减少可能是由于放大的神经祖细胞 (ANP) 的死亡增加。此外,星形胶质细胞变得具有反应性,小胶质细胞在几乎所有研究的海马区域中的数量都增加了。胶质细胞变化导致非炎症反应,因为主要促炎细胞因子(IL-1β、TNFα、IL-18)的 mRNA 保持不变,但 CD200R mRNA 水平下调。SCI 后长期,星形胶质细胞保持反应性,但另一方面,小胶质细胞密度降低。此外,胶质细胞诱导神经炎症环境,IL-1β、TNFα和IL-18 mRNA表达上调,CD200R mRNA减少。神经发生减少可能在后来的时间点归因于神经干细胞 (NSC) 的失活和 ANP 增殖的抑制。颗粒细胞和CA1锥体神经元的数量仅在慢性期减少。慢性期促炎细胞因子的释放可能涉及神经发生减少和海马神经元的神经变性。所以,

更新日期:2020-06-14
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