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Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice

Standard

Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice. / Rolf, Bettina; Bastmeyer, Martin; Schachner, Melitta; Bartsch, Udo.

in: J NEUROSCI, Jahrgang 22, Nr. 19, 01.10.2002, S. 8357-62.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Rolf, B, Bastmeyer, M, Schachner, M & Bartsch, U 2002, 'Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice', J NEUROSCI, Jg. 22, Nr. 19, S. 8357-62.

APA

Rolf, B., Bastmeyer, M., Schachner, M., & Bartsch, U. (2002). Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice. J NEUROSCI, 22(19), 8357-62.

Vancouver

Rolf B, Bastmeyer M, Schachner M, Bartsch U. Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice. J NEUROSCI. 2002 Okt 1;22(19):8357-62.

Bibtex

@article{aa3749b1ed4c4f06b7cf71334f4571d6,
title = "Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice",
abstract = "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.",
keywords = "Animals, Animals, Newborn, Axons, Immunohistochemistry, Mice, Mice, Mutant Strains, Nervous System Malformations, Neural Cell Adhesion Molecules, Pyramidal Tracts, Sialic Acids, Thiazines, Journal Article, Research Support, Non-U.S. Gov't",
author = "Bettina Rolf and Martin Bastmeyer and Melitta Schachner and Udo Bartsch",
year = "2002",
month = oct,
day = "1",
language = "English",
volume = "22",
pages = "8357--62",
journal = "J NEUROSCI",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "19",

}

RIS

TY - JOUR

T1 - Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice

AU - Rolf, Bettina

AU - Bastmeyer, Martin

AU - Schachner, Melitta

AU - Bartsch, Udo

PY - 2002/10/1

Y1 - 2002/10/1

N2 - 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.

AB - 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.

KW - Animals

KW - Animals, Newborn

KW - Axons

KW - Immunohistochemistry

KW - Mice

KW - Mice, Mutant Strains

KW - Nervous System Malformations

KW - Neural Cell Adhesion Molecules

KW - Pyramidal Tracts

KW - Sialic Acids

KW - Thiazines

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

M3 - SCORING: Journal article

C2 - 12351709

VL - 22

SP - 8357

EP - 8362

JO - J NEUROSCI

JF - J NEUROSCI

SN - 0270-6474

IS - 19

ER -