Table 1.

Summary of various approaches used to neutralize NgR1

Strategy	In vitro		In vivo
Strategy	GC collapse	Neurite outgrowth	Axon regeneration	Behavioral recovery
NEP1–40^a	E12 chick DRG with Nogo-66	E12 chick DRG on myelin	Corticospinal tract	Locomotor
NgR(1–310)ecto^b, ^c	ND	E13 chick DRGs on Nogo-66 and myelin	Corticospinal and raphespinal tracts	Locomotor
DN-NgR1^d, ^e	ND	P7–P9 mouse CGNs on Nogo-66, MAG, OMGp, and myelin	Growth-stimulated retinal ganglion cells	ND
NgR1-null mice^f, ^g	P6 DRGs with Nogo-66, MAG, OMGp, and myelin	ND	Raphespinal and rubrospinal tracts^f and corticospinal fibers^g	Locomotor^f
NgR1-null mice^h	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.
↵^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.