作者: Fred Winter , Anthony J. G. D. Holtmaat , Joost Verhaagen
DOI: 10.1007/978-1-4615-0119-0_10
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摘要: Injury to the mature mammalian central nervous system (CNS) is often accompanied by permanent loss of function damaged neural circuits. The failure injured CNS axons regenerate thought be caused, in part, neurite outgrowth inhibitory factors expressed and around lesion. These include several myelin associated inhibitors, proteoglycans, tenascin-R. Recent studies have documented presence class 3 semaphorins fibroblast-like meningeal cells present core scar formed following injury. Class display growth-inhibitory effects on growing during embryonic development. induction expression persistent their receptors, neuropilins plexins, neurons suggest that they contribute regenerative neurons. Neuropilins are also a subpopulation fibroblast vicinity scar. Semaphorin/neuropilin signaling might therefore important for cell migration, angiogenis neuronal death or scars. In contrast CNS, neuropilin/plexin positive PNS do long distance regeneration Injured not encounter semaphorin Furthermore, Semaphorin 3A downregulated regenerating spinal motor themselves. This was transient upregulation target muscle. observations injury induced regulation contributes successful reinnervation. Future genetically modified mice should provide more insight into mechanisms which influence degeneration.