Table 1.

Summary of various approaches used to neutralize NgR1

StrategyIn vitroIn vivo
GC collapseNeurite outgrowthAxon regenerationBehavioral recovery
NEP1–40aE12 chick DRG with Nogo-66E12 chick DRG on myelinCorticospinal tractLocomotor
NgR(1–310)ectob, cNDE13 chick DRGs on Nogo-66 and myelinCorticospinal and raphespinal tractsLocomotor
DN-NgR1d, eNDP7–P9 mouse CGNs on Nogo-66, MAG, OMGp, and myelinGrowth-stimulated retinal ganglion cellsND
NgR1-null micef, gP6 DRGs with Nogo-66, MAG, OMGp, and myelinNDRaphespinal and rubrospinal tractsf and corticospinal fibersgLocomotorf
NgR1-null micehNDNo reversal for P7 CGNs and P10 DRG neurons on Nogo-66 and myelinNo corticospinal tract regenerationNo 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.

  • aGrandPre et al., 2002.

  • bFournier et al., 2002.

  • cLi et al., 2004.

  • dWang et al., 2002.

  • eFischer et al., 2004.

  • fKim et al., 2004.

  • gCafferty and Strittmatter, 2006.

  • hZheng et al., 2005.