FIGURE 3 | Changes in CNS environments after maturation and injury.

From the following article:

Glial inhibition of CNS axon regeneration

Glenn Yiu and Zhigang He

Nature Reviews Neuroscience 7, 617-627 (August 2006)

doi:10.1038/nrn1956

Glial inhibition of CNS axon regeneration

During embryonic development, unmyelinated axons with motile growth cones can extend, retract and respond to various trophic and guidance molecules. This dynamic process allows the neural circuitry to be fine-tuned (a). As the nervous system matures after birth, myelination is finalized with oligodendrocytes ensheathing axons to prevent aberrant sprouting and astrocytes secreting chondroitin sulphate proteoglycans (CSPGs) to further limit structural plasticity in the adult (b). After CNS injury, axons become transected and reactive astrocytes further upregulate their secretion of CSPGs. The distal endings of severed axons form dystrophic growth cones and become exposed to CSPGs from the glial scar, as well as myelin-associated inhibitors from oligodendrocytes and myelin debris (c). As similar mechanisms prevent short-range plasticity in the adult and long-distance axon repair after injury, relieving these inhibitory influences might not only enhance the regeneration of severed axons, but might also promote compensatory sprouting. EphA4, the cognate neuronal receptor for ephrin B3; MAG, myelin-associated glycoprotein; NgR, Nogo-66 receptor; OMgp, oligodendrocyte myelin glycoprotein; Trk, tyrosine receptor kinase.

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