QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Rolf, B. Articles by Bartsch, U. Search for Related Content PubMed PubMed Citation Articles by Rolf, B. Articles by Bartsch, U.

 Previous Article  |  Next Article 

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

---

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

This article has been cited by other articles:

				W. J. Brackenbury, T. H. Davis, C. Chen, E. A. Slat, M. J. Detrow, T. L. Dickendesher, B. Ranscht, and L. L. Isom Voltage-Gated Na+ Channel {beta}1 Subunit-Mediated Neurite Outgrowth Requires Fyn Kinase and Contributes to Postnatal CNS Development In Vivo J. Neurosci., March 19, 2008; 28(12): 3246 - 3256. [Abstract] [Full Text] [PDF]

				B. Weinhold, R. Seidenfaden, I. Rockle, M. Muhlenhoff, F. Schertzinger, S. Conzelmann, J. D. Marth, R. Gerardy-Schahn, and H. Hildebrandt Genetic Ablation of Polysialic Acid Causes Severe Neurodevelopmental Defects Rescued by Deletion of the Neural Cell Adhesion Molecule J. Biol. Chem., December 30, 2005; 280(52): 42971 - 42977. [Abstract] [Full Text] [PDF]

				T. H. Davis, C. Chen, and L. L. Isom Sodium Channel {beta}1 Subunits Promote Neurite Outgrowth in Cerebellar Granule Neurons J. Biol. Chem., December 3, 2004; 279(49): 51424 - 51432. [Abstract] [Full Text] [PDF]

				D. G.M. Molin, R. E. Poelmann, M. C. DeRuiter, M. Azhar, T. Doetschman, and A. C. Gittenberger-de Groot Transforming Growth Factor {beta}-SMAD2 Signaling Regulates Aortic Arch Innervation and Development Circ. Res., November 26, 2004; 95(11): 1109 - 1117. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help