Loss of neural recognition molecule NB‐3 delays the normal projection and terminal branching of developing corticospinal tract axons in the mouse

Neural recognition molecule NB‐3 is involved in neural development and synapse formation. However, its role in axon tract formation is unclear. In this study, we found that the temporal expression of NB‐3 in the deep layers of the motor cortex in mice was coincident with the development of the corticospinal tract (CST). Clear NB‐3 immunoreactivity in the CST trajectory strongly suggested that NB‐3 was expressed specifically in projecting CST axons. By tracing CST axons in NB‐3−/− mice at different developmental stages, we found that these axons were capable of projecting and forming a normal trajectory. However, the projection was greatly delayed in NB‐3−/− mice compared with wild‐type (WT) mice from the embryonic to postnatal stages, a period that is coincident with the completion of the CST projection in mice. Subsequently, although their projection was delayed, CST axons in NB‐3−/− mice gradually completed a normal projection. By stage P21, the characteristics of CST projections in NB‐3−/− mice were not statistically different from those in WT mice. In addition, we found that the branching of CST axons into spinal gray matter also was delayed in NB‐3−/− mice. The CST innervation area in the spinal gray matter of NB‐3−/− mice was greatly reduced in comparison with WT mice until P30 and gradually became normal by P45. These data suggest that NB‐3 is involved in the normal projection and terminal branching of developing CST axons. J. Comp. Neurol. 520:1227–1245, 2012. © 2011 Wiley Periodicals, Inc.

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