Abstract
Whether or not the postnatal mammalian brain is capable of any level of self-repair following injury, remains a fundamental but unanswered question in regenerative neurobiology. Ischemic damage to the rodent forebrain has been widely used as a model system, where there have been contradictory reports regarding the capacity of the brain to replace striatal projection neurons. Here we used a software-assisted, confocal approach to survey thousands of cells generated after striatal ischemic injury and showed that not only does injury fail to stimulate production of new striatal projection neurons in the adult brain, but it also fails to do so in the early postnatal brain. 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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
