FIGURE 2 | Glial inhibitors and intracellular signalling mechanisms.
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
The molecular inhibitors of the adult CNS glial environment include chondroitin sulphate proteoglycans (CSPGs) associated with reactive astrocytes from the glial scar43, and myelin-associated inhibitors from intact oligodendrocytes and myelin debris, including myelin-associated glycoprotein (MAG)22, 23, Nogo-A14, 15, 16, oligodendrocyte myelin glycoprotein (OMgp)24, ephrin B3 (Ref. 26) and the transmembrane semaphorin 4D (Sema4D)25. Although the topology of Nogo-A remains unclear, both the 66 amino acid loop (Nogo-66) and the amino-terminal domain (amino-Nogo) are known to be inhibitory to axon outgrowth14, 15, 18, 19. The neuronal receptors and downstream signalling pathways known to be involved in transducing these inhibitory signals are shown. Among the signalling components that are common to both CSPG and myelin inhibition are the activation of RhoA82 and the rise in intracellular calcium65, 89, 92, 93. Whereas the signals downstream of RhoA that lead to the actin cytoskeleton are well characterized (solid arrows), the relationship between components upstream of RhoA and the role of calcium influx are still ambiguous (dashed arrows). For example, calcium transients might activate protein kinase C (PKC)88, 89, which is required for p75 cleavage by 
-secretase66, or trigger the transactivation of epidermal growth factor receptor (EGFR)90.
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