Abstract
The localization of an axon growth inhibitory molecule Nogo and its receptor (NgR) was investigated in the mouse spinal cord during prenatal development of the commissural pathway. Using the antibody N18, an intense signal for Nogo was localized largely on radial glia processes that are immunoreactive to RC2 antibody during the major period of commissural axon growth and was gradually reduced towards the end of gestation. The glial processes ramified extensively in the ventral funiculus and resided within the interfascicular space between the longitudinally projecting axons. Axonal localization of Nogo was observed on the premidline segment of commissural axons and on axons in the dorsal and ventral funiculi, but only at the earliest stage of pathway development. Nogo signals were initially weak on the glial processes during the period of axon crossing in the floor plate but was elevated when the decussation is finished. NgR was expressed on the commissural axons; the expression pattern is spatially regulated, being low in the premidline and midline courses but is upregulated when the axons leave the floor plate. These expression patterns raise the possibilities that the glial-specific form of Nogo may be involved in the guidance of commissural axons by (i) preventing recrossing of axons across the midline through an upregulation of axonal NgR and (ii) partitioning axons in the ventral funiculus into longitudinal fascicles.