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创伤性脑损伤与海马神经发生:功能意义。

Traumatic brain injury and hippocampal neurogenesis: Functional implications.

机构信息

The Department of Neurobiology and Anatomy, University of Texas McGovern Medical School, Houston, TX 77030, United States of America.

The Department of Neurobiology and Anatomical Sciences, University of Mississippi Medical Center, United States of America.

出版信息

Exp Neurol. 2020 Sep;331:113372. doi: 10.1016/j.expneurol.2020.113372. Epub 2020 Jun 3.

Abstract

In the adult brain, self-renewing radial-glia like (RGL) progenitor cells have been shown to reside in the subventricular zone and the subgranular zone of the hippocampus. A large body of evidence shows that experiences such as learning, enriched environment and stress can alter proliferation and differentiation of RGL progenitor cells. The progenitor cells present in the subgranular zone of the hippocampus divide to give rise to newborn neurons that migrate to the dentate gyrus where they differentiate into adult granule neurons. These newborn neurons have been found to have a unique role in certain types of hippocampus-dependent learning and memory, including goal-directed behaviors that require pattern separation. Experimental traumatic brain injury (TBI) in rodents has been shown to alter hippocampal neurogenesis, including triggering the acute loss of newborn neurons, as well as progenitor cell hyper-proliferation. In this review, we discuss the role of hippocampal neurogenesis in learning and memory. Furthermore, we review evidence for the molecular mechanisms that contribute to newborn neuron loss, as well as increased progenitor cell proliferation after TBI. Finally, we discuss strategies aimed at enhancing neurogenesis after TBI and their possible therapeutic benefits.

摘要

在成人的大脑中,自我更新的放射状胶质样(RGL)祖细胞被证明存在于脑室下区和海马的颗粒下区。大量证据表明,学习、丰富的环境和压力等经历可以改变 RGL 祖细胞的增殖和分化。海马颗粒下区存在的祖细胞分裂产生新的神经元,这些神经元迁移到齿状回,在那里分化为成年颗粒神经元。这些新生神经元被发现具有在某些类型的海马依赖学习和记忆中独特的作用,包括需要模式分离的目标导向行为。实验性创伤性脑损伤(TBI)在啮齿动物中已被证明会改变海马神经发生,包括引发新生神经元的急性丢失,以及祖细胞的过度增殖。在这篇综述中,我们讨论了海马神经发生在学习和记忆中的作用。此外,我们还回顾了导致 TBI 后新生神经元丢失以及祖细胞增殖增加的分子机制的证据。最后,我们讨论了旨在增强 TBI 后神经发生的策略及其可能的治疗益处。

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