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The Journal of Neuroscience, October 1, 2002, 22(19):8357-8362

BRIEF COMMUNICATION
Pathfinding Errors of Corticospinal Axons in Neural Cell Adhesion Molecule-Deficient Mice

Bettina Rolf¹, Martin Bastmeyer², Melitta Schachner¹, and Udo Bartsch¹

¹ Zentrum für Molekulare Neurobiologie, Universität Hamburg, D-20246 Hamburg, Germany, and ² Fachbereich Biologie, Universität Konstanz, D-78457 Konstanz, Germany

The neural cell adhesion molecule (NCAM) is a cell recognition molecule of the Ig superfamily implicated in cell migration, myelination, and synaptic plasticity, as well as elongation, fasciculation, and pathfinding of axons. Here, we used NCAM-deficient mice to investigate the role of NCAM in the development of the corticospinal tract. We demonstrate severe hypoplasia of the corticospinal tract in adult NCAM mutants. Anterograde tracing of the tract of early postnatal NCAM mutants revealed pronounced pathfinding errors of corticospinal axons. At the pyramidal decussation of mutant mice, some corticospinal axons either stayed ventrally and extended laterally, or axons turned dorsally, but instead of growing to the contralateral dorsal column, a significant fraction of axons projected ipsilaterally. We also observed that corticospinal axons of NCAM mutants entered the pyramidal decussation significantly later than axons of wild-type littermates. Our observations thus demonstrate a critical role of NCAM for the formation of this major axon tract.

Key words: adhesion molecule; axonal pathfinding; corticospinal tract; mouse; NCAM; polysialic acid

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22198357-06$05.00/0

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