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The role of L1 in axon pathfinding and fasciculation

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The role of L1 in axon pathfinding and fasciculation. / Wiencken-Barger, A E; Mavity-Hudson, J; Bartsch, U; Schachner, M; Casagrande, V A.

in: CEREB CORTEX, Jahrgang 14, Nr. 2, 02.2004, S. 121-31.

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

Harvard

Wiencken-Barger, AE, Mavity-Hudson, J, Bartsch, U, Schachner, M & Casagrande, VA 2004, 'The role of L1 in axon pathfinding and fasciculation', CEREB CORTEX, Jg. 14, Nr. 2, S. 121-31.

APA

Wiencken-Barger, A. E., Mavity-Hudson, J., Bartsch, U., Schachner, M., & Casagrande, V. A. (2004). The role of L1 in axon pathfinding and fasciculation. CEREB CORTEX, 14(2), 121-31.

Vancouver

Wiencken-Barger AE, Mavity-Hudson J, Bartsch U, Schachner M, Casagrande VA. The role of L1 in axon pathfinding and fasciculation. CEREB CORTEX. 2004 Feb;14(2):121-31.

Bibtex

@article{34aaaba031b34ad981374a6e68e39e4d,
title = "The role of L1 in axon pathfinding and fasciculation",
abstract = "The neural cell adhesion molecule L1 has been found to play important roles in axon growth and fasciculation. Our main objective was to determine the role of L1 during the development of connections between thalamus and cortex. We find that thalamocortical and corticothalamic axons in mice lacking L1 are hyperfasciculated, a subset of thalamocortical axons make pathfinding errors and thalamocortical axon growth cones are abnormally long in the subplate. These defects occur despite formation of six cortical layers and formation of topographically appropriate thalamocortical connections. The loss of L1 is accompanied by loss of expression of ankyrin-B, an intracellular L1 binding partner, suggesting that L1 is involved in the regulation of Ank2 stability. We postulate that the pathfinding errors, growth cone abnormalities and hyperfasciculation of axons following loss of L1 reflect both a shift in binding partners among axons and different substrates and a loss of appropriate interactions with the cytoskeleton.",
keywords = "Animals, Axons, Cerebral Cortex, Female, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neural Cell Adhesion Molecule L1, Neural Cell Adhesion Molecules, Neural Pathways, Thalamus, Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.",
author = "Wiencken-Barger, {A E} and J Mavity-Hudson and U Bartsch and M Schachner and Casagrande, {V A}",
year = "2004",
month = feb,
language = "English",
volume = "14",
pages = "121--31",
journal = "CEREB CORTEX",
issn = "1047-3211",
publisher = "Oxford University Press",
number = "2",

}

RIS

TY - JOUR

T1 - The role of L1 in axon pathfinding and fasciculation

AU - Wiencken-Barger, A E

AU - Mavity-Hudson, J

AU - Bartsch, U

AU - Schachner, M

AU - Casagrande, V A

PY - 2004/2

Y1 - 2004/2

N2 - The neural cell adhesion molecule L1 has been found to play important roles in axon growth and fasciculation. Our main objective was to determine the role of L1 during the development of connections between thalamus and cortex. We find that thalamocortical and corticothalamic axons in mice lacking L1 are hyperfasciculated, a subset of thalamocortical axons make pathfinding errors and thalamocortical axon growth cones are abnormally long in the subplate. These defects occur despite formation of six cortical layers and formation of topographically appropriate thalamocortical connections. The loss of L1 is accompanied by loss of expression of ankyrin-B, an intracellular L1 binding partner, suggesting that L1 is involved in the regulation of Ank2 stability. We postulate that the pathfinding errors, growth cone abnormalities and hyperfasciculation of axons following loss of L1 reflect both a shift in binding partners among axons and different substrates and a loss of appropriate interactions with the cytoskeleton.

AB - The neural cell adhesion molecule L1 has been found to play important roles in axon growth and fasciculation. Our main objective was to determine the role of L1 during the development of connections between thalamus and cortex. We find that thalamocortical and corticothalamic axons in mice lacking L1 are hyperfasciculated, a subset of thalamocortical axons make pathfinding errors and thalamocortical axon growth cones are abnormally long in the subplate. These defects occur despite formation of six cortical layers and formation of topographically appropriate thalamocortical connections. The loss of L1 is accompanied by loss of expression of ankyrin-B, an intracellular L1 binding partner, suggesting that L1 is involved in the regulation of Ank2 stability. We postulate that the pathfinding errors, growth cone abnormalities and hyperfasciculation of axons following loss of L1 reflect both a shift in binding partners among axons and different substrates and a loss of appropriate interactions with the cytoskeleton.

KW - Animals

KW - Axons

KW - Cerebral Cortex

KW - Female

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Neural Cell Adhesion Molecule L1

KW - Neural Cell Adhesion Molecules

KW - Neural Pathways

KW - Thalamus

KW - Comparative Study

KW - Journal Article

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

KW - Research Support, U.S. Gov't, P.H.S.

M3 - SCORING: Journal article

C2 - 14704209

VL - 14

SP - 121

EP - 131

JO - CEREB CORTEX

JF - CEREB CORTEX

SN - 1047-3211

IS - 2

ER -