Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice
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Pathfinding errors of corticospinal axons in neural cell adhesion molecule-deficient mice. / Rolf, Bettina; Bastmeyer, Martin; Schachner, Melitta; Bartsch, Udo.
In: J NEUROSCI, Vol. 22, No. 19, 01.10.2002, p. 8357-62.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -