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本文引用的文献

1
Enhanced cued fear memory following post-training whole body irradiation of 3-month-old mice.3个月大小鼠训练后全身照射增强线索性恐惧记忆。
Behav Brain Res. 2017 Feb 15;319:181-187. doi: 10.1016/j.bbr.2016.11.031. Epub 2016 Nov 16.
2
Juvenile striatal white matter is resistant to ischemia-induced damage.青少年纹状体白质对缺血性损伤具有抗性。
Glia. 2016 Nov;64(11):1972-86. doi: 10.1002/glia.23036. Epub 2016 Jul 27.
3
Use of the Open Field Maze to measure locomotor and anxiety-like behavior in mice.使用旷场迷宫来测量小鼠的运动能力和焦虑样行为。
J Vis Exp. 2015 Feb 6(96):e52434. doi: 10.3791/52434.
4
Post-stroke cognitive impairment: epidemiology, mechanisms and management.脑卒中后认知障碍:流行病学、发病机制与管理。
Ann Transl Med. 2014 Aug;2(8):80. doi: 10.3978/j.issn.2305-5839.2014.08.05.
5
Neurogenesis and inflammation after ischemic stroke: what is known and where we go from here.缺血性脑卒中后的神经发生和炎症:已知的和未来的方向。
J Cereb Blood Flow Metab. 2014 Oct;34(10):1573-84. doi: 10.1038/jcbfm.2014.130. Epub 2014 Jul 30.
6
Radiation exposure prior to traumatic brain injury induces responses that differ as a function of animal age.颅脑损伤前的辐射暴露会引起不同的反应,其反应程度取决于动物的年龄。
Int J Radiat Biol. 2014 Mar;90(3):214-23. doi: 10.3109/09553002.2014.859761. Epub 2014 Feb 6.
7
MicroRNAs in cerebral ischemia-induced neurogenesis.脑缺血诱导神经发生中的 microRNAs。
J Neuropathol Exp Neurol. 2013 Aug;72(8):718-22. doi: 10.1097/NEN.0b013e31829e4963.
8
Experimental pediatric arterial ischemic stroke model reveals sex-specific estrogen signaling.实验性儿科动脉缺血性中风模型揭示了性别特异性的雌激素信号。
Stroke. 2013 Mar;44(3):759-63. doi: 10.1161/STROKEAHA.112.675124. Epub 2013 Jan 24.
9
Phenotyping the function of TRPV1-expressing sensory neurons by targeted axonal silencing.通过靶向轴突沉默来表型 TRPV1 表达感觉神经元的功能。
J Neurosci. 2013 Jan 2;33(1):315-26. doi: 10.1523/JNEUROSCI.2804-12.2013.
10
Assessing post-stroke behavior in mouse models of focal ischemia.评估局灶性缺血小鼠模型的卒中后行为。
J Cereb Blood Flow Metab. 2013 Mar;33(3):330-8. doi: 10.1038/jcbfm.2012.185. Epub 2012 Dec 12.

脑缺血后幼年大脑中的内源性神经元替代。

Endogenous Neuronal Replacement in the Juvenile Brain Following Cerebral Ischemia.

机构信息

Department of Anesthesiology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, United States; Department of Pharmacology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, United States; Neuronal Injury Program, University of Colorado Denver, Anschutz Medial Campus, Aurora, CO 80045, United States.

Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO 80045, United States.

出版信息

Neuroscience. 2018 Jun 1;380:1-13. doi: 10.1016/j.neuroscience.2018.03.045. Epub 2018 Apr 9.

DOI:10.1016/j.neuroscience.2018.03.045
PMID:29649514
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5943176/
Abstract

Replacement of dead neurons following ischemia, either via enhanced endogenous neurogenesis or stem cell therapy, has long been sought. Unfortunately, while various therapies that enhance neurogenesis or stem cell therapies have proven beneficial in animal models, they have all uniformly failed to truly replace dead neurons in the ischemic core to facilitate long-term recovery. Remarkably, we observe robust repopulation of medium-spiny neurons within the ischemic core of juvenile mice following experimental stroke. Despite extensive neuronal cell death in the injured striatum of both juveniles and adults at acute time points after ischemia (24 h and 7 d), mature newborn neurons replaced lost striatal neurons at 30 d post-ischemia. This neuronal repopulation was found only in juveniles, not adults, and importantly, was accompanied by enhanced post-ischemic behavioral recovery at 30 d. Ablation of neurogenesis using irradiation prevented neuronal replacement and functional recovery in MCAo-injured juvenile mice. In contrast, findings in adults were consistent with previous reports, that newborn neurons failed to mature and died, offering little therapeutic potential. These data provide support for neuronal replacement and consequent functional recovery following ischemic stroke and new targets in the development of novel therapies to treat stroke.

摘要

长期以来,人们一直希望通过增强内源性神经发生或干细胞疗法来替代缺血后死亡的神经元。不幸的是,尽管各种增强神经发生或干细胞疗法的治疗方法已被证明在动物模型中是有益的,但它们都未能真正替代缺血核心中的死亡神经元,从而促进长期恢复。值得注意的是,我们观察到实验性中风后幼鼠缺血核心内中型多棘神经元的大量再殖。尽管在缺血后急性时间点(24 小时和 7 天),幼鼠和成年鼠的损伤纹状体中存在广泛的神经元死亡,但成熟的新生神经元在缺血后 30 天取代了丢失的纹状体神经元。这种神经元再殖仅发生在幼鼠中,而不是成年鼠中,重要的是,这伴随着缺血后 30 天行为恢复的增强。使用辐照进行神经发生消融可防止 MCAo 损伤的幼鼠中的神经元替代和功能恢复。相比之下,成年鼠的发现与之前的报告一致,即新生神经元未能成熟并死亡,几乎没有治疗潜力。这些数据为缺血性中风后神经元替代和随后的功能恢复提供了支持,并为开发治疗中风的新疗法提供了新的目标。