Department of Medicine, School of Medicine, University of Minnesota, 401 East River Parkway, Minneapolis, MN 55455, USA.
Department of Neurology, School of Medicine, Yale University, 300 George Street, New Haven, CT 06511, USA; Department of Pharmacology, School of Medicine, Yale University, 333 Cedar Street, New Haven, CT 06520, USA; Equal contribution.
Trends Mol Med. 2018 Jul;24(7):615-629. doi: 10.1016/j.molmed.2018.05.007. Epub 2018 Jun 19.
Genome-wide screens, proteomics, and candidate-based approaches have identified numerous genes associated with neuronal regeneration following central nervous system (CNS) injury. Despite significant progress, functional recovery remains a challenge, even in model systems. Neuronal function depends on segregation of axonal versus dendritic domains. A key to functional recovery may lie in recapitulating the developmental signals that instruct axon specification and growth in adult neurons post-injury. Theoretically, binary activator-inhibitor elements operating as a Turing-like system within neurons can specify axonal versus dendritic domains and promote axon growth. We review here various molecules implicated in axon specification that function as signaling pairs driving neuronal polarization and axon growth.
全基因组筛选、蛋白质组学和基于候选基因的方法已经鉴定出许多与中枢神经系统 (CNS) 损伤后神经元再生相关的基因。尽管取得了重大进展,但功能恢复仍然是一个挑战,即使在模型系统中也是如此。神经元的功能取决于轴突与树突域的分离。功能恢复的关键可能在于重现发育信号,这些信号在损伤后指导成年神经元中的轴突特化和生长。从理论上讲,作为神经元内类似于图灵系统的二元激活-抑制元件可以指定轴突与树突域,并促进轴突生长。在这里,我们回顾了各种参与轴突特化的分子,这些分子作为信号对,驱动神经元极化和轴突生长。