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. 2009 Jan 21;29(3):630–637. doi: 10.1523/JNEUROSCI.5204-08.2009

Figure 4.

Figure 4.

MAG mediated axonal stability via an NgR-independent pathway. a, NgR1 knock-out mice exhibited no evidence of Wallerian-like axonal degeneration (ai) or loss in axonal number (aii) within the medial dorsal column in C5 spinal cords or the sciatic nerve (harvested proximal to the bifurcation) at 12 months of age (n = 5 mice/group). b, MAG prevented axonal degeneration from vincristine in DRG neurons treated with PI-PLC. Coadministration of either Nogo or OMgp peptides, nonspecific NgR agonists, did not provide axonal protection against vincristine. Because MAG mediated axonal protection was unaltered by the inhibition of NgR with PI-PLC and activation of NgR by Nogo or OMgp did not confer axonal protection, our data suggest that MAG promotes axonal stability via an NgR-independent pathway. (*VIN+MAG-Fc vs VIN, VIN+MAG-Fc+PI-PLC vs VIN, Nogo vs VIN+ Nogo, Nogo+PI-PLC vs VIN+Nogo, n = 10 chambers/condition, p values <0.01). c, A MAG-Fc mutant with RGD altered to KGE (mtMAG) failed to prevent axonal degeneration from vincristine in primary DRG neuronal cultures (*VIN+wtMAG vs VIN, VIN+wtMAG vs VIN+mtMAG, n = 8 chambers/condition, p values <0.01). d, MAG did not promote axonal stability or prevent axonal degeneration in DRG cultures from B4galnt1 knock-out mice lacking complex gangliosides. (n = 8 chambers/condition).