Axon regeneration and the sprouting processes that underlie plasticity are blocked by inhibitory factors in the central nervous system (CNS) environment, several of which are upregulated after injury. The major inhibitory molecules are those associated with myelin and those associated with the glial scar. In myelin, NogoA, MAG, and OMgp are present on normal oligodendrocytes and on myelin debris. They act partly via the Nogo receptor, partly via an unidentified amino-Nogo receptor. In the glial scar, chondroitin sulphate proteoglycans, semaphorins, and the formation of a collagen-based membrane are all inhibitory. Methods to counteract these forms of inhibition have been identified, and these treatments promote axon regeneration in the damaged spinal cord, and in some cases recovery of function through enhanced plasticity.
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