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Strategy In vitro In vivo GC collapse Neurite outgrowth Axon regeneration Behavioral recovery NEP1–40a E12 chick DRG with Nogo-66 E12 chick DRG on myelin Corticospinal tract Locomotor NgR(1–310)ectob, c ND E13 chick DRGs on Nogo-66 and myelin Corticospinal and raphespinal tracts Locomotor DN-NgR1d, e ND P7–P9 mouse CGNs on Nogo-66, MAG, OMGp, and myelin Growth-stimulated retinal ganglion cells ND NgR1-null micef, g P6 DRGs with Nogo-66, MAG, OMGp, and myelin ND Raphespinal and rubrospinal tractsf and corticospinal fibersg Locomotorf NgR1-null miceh ND No reversal for P7 CGNs and P10 DRG neurons on Nogo-66 and myelin No corticospinal tract regeneration No recovery -
To assess the effects of NgR1 on long-distance regeneration and functional recovery in CNS injury models, NgR1 activity has been neutralized by several approaches. The small Nogo-66 (1–40) antagonist peptide (NEP 1–40) is a competitive antagonist of the Nogo-66 binding site of NgR. The soluble ligand-binding domain of NgR1 [NgR(310)ecto] cannot interact with coreceptors. A dominant-negative form of NgR (DN-NgR) lacks the last 136 aa in the C-terminal domain, which prevents NgR1 binding to coreceptors such as p75. Most of the neurons used in these studies are cerebellar granule neurons (CGNs) and DRG neurons. E, Embryonic day; ND, not determined.
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↵eFischer et al., 2004.
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