Summary
Successful axon regeneration requires injured neurons upregulate a specific set of growth-associated genes needed to sustain long-distance neuritic elongation. Most of these genes are active during axonogenesis, but they are downregulated at the end of development following the appearance of environmental inhibitory cues. In the mammalian CNS, these cues include molecules issued by target cells or non-neuronal elements localized along the axon, including oligodendrocytes. The extrinsic inhibitory activity can be overcome when the neuronal expression of growth genes is enhanced or following manipulations that shift the balance between attractive and repulsive signalling pathways in the growth cone. Nevertheless, neutralisation of inhibitory molecules in the intact CNS induces aberrant axon growth, indicating that a major physiological function of these molecules is to restrain neuritic plasticity in order to maintain connection specificity.
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Rossi, F. (2004). Regulation of the Intrinsic Growth Properties in Mammalian Neurons. In: Herdegen, T., Delgado-GarcÃa, J. (eds) Brain Damage and Repair. Springer, Dordrecht. https://doi.org/10.1007/1-4020-2541-6_22
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