Nogo‐B is the major form of Nogo at the floor plate and likely mediates crossing of commissural axons in the mouse spinal cord
Nogo is a myelin associated protein that belongs to the reticulon superfamily proteins. It exists in at least three known isoforms, Nogo‐A, ‐B, and ‐C (GrandPre, Nakamura, Vartanian, & Strittmatter, 2000). In the adult central nervous system (CNS), Nogo is found in the myelin sheath and cell bodies of oligodendrocytes (Huber, Weinmann, Brosamle, Oertle, & Schwab, 2002; Kuhlmann, Remington, Maruschak, Owens, & Bruck, 2007). Nogo's inhibitory action on axon regeneration after CNS injuries has been studied extensively. The inhibitory effects of Nogo act through binding to the Nogo receptor (NgR) complex (Domeniconi et al., 2002; Wang et al., 2002). However, Nogo is also expressed in subsets of neurons in the adult CNS (Cheatwood, Emerick, Schwab, & Kartje, 2008; Huber et al., 2002), indicating functions other than inhibiting axon growth.
In our recent studies, Nogo, in particularly Nogo‐B, was shown to be expressed by the radial glia at the midline of mouse chiasm (Wang, Chan, Taylor, & Chan, 2008b; Wang, Wang, Ma, Taylor, & Chan, 2016). It contributes to the bilateral routing of optic axons through differential regulation of NgR expression on the nasal and ventral temporal axons at the chiasm (Wang, Chan, Taylor, & Chan, 2008a). We have also shown that Nogo is expressed strongly on the radial glia at the ventral midline of mouse spinal cord when commissural axons are growing through the floor plate (Wang, Wang, Zhao, & Chan, 2010). The expression of NgR is spatially regulated, with a basal level on axons growing toward and navigating the floor plate, but at an elevated level on axons after crossing and joining the longitudinal tracts. This expression pattern suggests a role for Nogo in the post‐crossing phase. However, other studies have shown that Nogo is expressed largely in neurons and axons in the developing spinal cord rather than on glial cells (Caltharp et al., 2007; Huber et al., 2002; O'Neill, Whalley, & Ferretti, 2004), arguing against a role in axon guidance.