Ermine Charlotte M, Wright Jordan L, Stanic Davor, Parish Clare L, Thompson Lachlan H
The Florey Institute for Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3052, Australia.
The Florey Institute for Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3052, Australia.
iScience. 2020 Jun 26;23(6):101175. doi: 10.1016/j.isci.2020.101175. Epub 2020 May 18.
Ischemic damage to the adult rodent forebrain has been widely used as a model system to study injury-induced neurogenesis, resulting in contradictory reports regarding the capacity of the postnatal brain to replace striatal projection neurons. Here we used a software-assisted, confocal approach to survey thousands of cells generated after striatal ischemic injury in rats and showed that injury fails not only to stimulate production of new striatal projection neurons in the adult brain but also to do so in the neonatal brain at early postnatal ages not previously explored. Conceptually this is significant, because it shows that even during periods of active striatal neurogenesis, injury is not a sufficient stimulus to promote replacement of these neurons. Understanding the intrinsic capacity of the postnatal brain to replace neurons in response to injury is fundamental to the development of "self-repair" therapies.
成年啮齿动物前脑的缺血性损伤已被广泛用作研究损伤诱导神经发生的模型系统，这导致了关于出生后大脑替换纹状体投射神经元能力的相互矛盾的报道。在这里，我们使用了一种软件辅助的共聚焦方法来检测大鼠纹状体缺血损伤后产生的数千个细胞，并表明损伤不仅未能刺激成年大脑中产生新的纹状体投射神经元，而且在以前未探索的出生后早期的新生大脑中也未能做到这一点。从概念上讲，这很重要，因为它表明即使在纹状体神经发生活跃的时期，损伤也不是促进这些神经元替换的充分刺激因素。了解出生后大脑响应损伤替换神经元的内在能力是“自我修复”疗法发展的基础。
