中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (3): 469-470.doi: 10.4103/1673-5374.380883

• 观点:神经损伤修复保护与再生 •    下一篇

白质损伤后轴突-少突胶质细胞过早相互作用导致实验性轴突再生停滞

  

  • 出版日期:2024-03-15 发布日期:2023-09-01

Premature axon-oligodendrocyte interaction contributes to stalling of experimental axon regeneration after injury to the white matter

Ephraim F. Trakhtenberg*   

  1. Department of Neuroscience, University of Connecticut School of Medicine, Farmington, CT, USA
  • Online:2024-03-15 Published:2023-09-01
  • Contact: Ephraim F. Trakhtenberg, PhD, trakhtenberg@uchc.edu.
  • Supported by:
    This work was supported by grants from The University of Connecticut School of Medicine (Start-Up Fund), the National Institutes of Health (NIH) (Grant R01-EY029739), the Connecticut Institute for the Brain and Cognitive Sciences (Research Seed Grant), and the BrightFocus Foundation (Grant G2017204) (all to EFT).

摘要: https://orcid.org/0000-0003-2844-4191 (Ephraim F. Trakhtenberg)

Abstract: Studies from nearly 3 decades ago suggested that, in the central nervous system (CNS), myelination of axons by oligodendrocytes not only helps improve axonal conductivity but also stabilizes circuitry (Colello and Schwab, 1994). Over the years, myelin sheaths produced by oligodendrocytes have been found to contain multiple molecules that are inhibitory to axonal growth (e.g., MAG, NogoA, OMgp, Semaphorins) (Yiu and He, 2006; Silver et al., 2014). After white matter injury in the adult CNS, myelin debris from damaged axons and dead oligodendrocytes accumulates in the forming glial scar and exposes these myelin-associated axon growth-inhibitory molecules to the injured axonal stumps, thereby contributing to the inhibition of axonal regrowth. During development, CNS axons reach their postsynaptic targets and stop growing before oligodendrocytes appear and myelinate them (Foran and Peterson, 1992; Dangata et al., 1996). Therefore, myelin-associated axon growth-inhibitory molecules interacting with already grown axons during myelination were thought to block axons from promiscuous sprouting and miswiring, thereby stabilizing neural circuitry in the CNS (Colello and Schwab, 1994).