Overcoming inhibitors in myelin to promote axonal regeneration
Section snippets
Discussion
The central nervous system (CNS) of adult mammals recovers very poorly from injury. Mature central neurons, such as those in the spinal cord, respond to injury with an initial period of growth but their growth cones soon collapse and their axons fail to regenerate to any significant degree [1], [2], [3]. There is no a priori reason for this failure, since lower vertebrates can regenerate a severed spinal cord [4]. Even in mammals, the inability to regrow axonal tracts is limited to the mature
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DL-3-n-butylphthalide promotes neuroplasticity and motor recovery in stroke rats
2017, Behavioural Brain ResearchCitation Excerpt :Nogo-A can activate intracellular components of Nogo signaling-RhoA and its downstream target Rho-associated kinase (ROCK); this ultimately results in growth cone collapse and inhibition of axonal regeneration [19]. Thus, it has been proposed that blockade of Nogo-A/NgR or RhoA/ROCK could enhance the rewiring and improve the functional outcome in stroke animals [20–22]. In this study, we demonstrated that after dl-NBP treatment for 2 weeks in our ischemic rats, there were more CST fibers crossing over the midline and sprouting into the denervated gray matter in the cervical spinal cord.
Central Nervous System and its Disease Models on a Chip
2015, Trends in Biotechnology