早年应激影响成年海马神经元再生的机制
发布时间:2018-08-01 11:58
【摘要】:成年海马神经元再生是指齿状回颗粒下区的神经干细胞发育为功能性神经元的过程。在生命的早期经历应激事件可损害成年期海马神经元再生,并引起学习记忆障碍。然而,目前关于早年应激影响成年海马神经元再生的机制研究主要集中在糖皮质激素及受体系统,其相关调节分子与机制有待深入研究。本文阐述了主要的应激因子(包括促肾上腺皮质激素释放激素及其受体等系统)在早年应激介导的成年海马神经元再生异常和海马重塑中的潜在作用。
[Abstract]:The regeneration of adult hippocampal neurons refers to the development of neural stem cells from the subgranular area of dentate gyrus into functional neurons. Experiencing stress events at the early stage of life can damage the regeneration of hippocampal neurons in adulthood and lead to learning and memory impairment. However, the mechanism of early stress affecting the regeneration of adult hippocampal neurons is mainly focused on glucocorticoid and receptor system, and the related regulatory molecules and mechanisms need to be further studied. This paper describes the potential role of major stress factors (including corticotropin-releasing hormone and its receptor systems) in the early stress-mediated abnormal regeneration of adult hippocampal neurons and hippocampal remodeling.
【作者单位】: 浙江大学医学院神经生物学系卫生部医学神经生物学重点实验室;
【基金】:中国自然科学基金面上项目(81471369)支持
【分类号】:B845.1
,
本文编号:2157502
[Abstract]:The regeneration of adult hippocampal neurons refers to the development of neural stem cells from the subgranular area of dentate gyrus into functional neurons. Experiencing stress events at the early stage of life can damage the regeneration of hippocampal neurons in adulthood and lead to learning and memory impairment. However, the mechanism of early stress affecting the regeneration of adult hippocampal neurons is mainly focused on glucocorticoid and receptor system, and the related regulatory molecules and mechanisms need to be further studied. This paper describes the potential role of major stress factors (including corticotropin-releasing hormone and its receptor systems) in the early stress-mediated abnormal regeneration of adult hippocampal neurons and hippocampal remodeling.
【作者单位】: 浙江大学医学院神经生物学系卫生部医学神经生物学重点实验室;
【基金】:中国自然科学基金面上项目(81471369)支持
【分类号】:B845.1
,
本文编号:2157502
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