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