Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice.

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Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice. / Weiss, Karl Heinz; Johanssen, Celine; Tielsch, Albrecht; Herz, Joachim; Deller, Thomas; Frotscher, Michael; Förster, Eckart.

In: J COMP NEUROL, Vol. 460, No. 1, 1, 2003, p. 56-65.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

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Weiss KH, Johanssen C, Tielsch A, Herz J, Deller T, Frotscher M et al. Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice. J COMP NEUROL. 2003;460(1):56-65. 1.

Bibtex

@article{c45dd25728fa4a60899b190b76dc37d8,
title = "Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice.",
abstract = "We studied the postnatal development of the radial glial scaffold in the dentate gyrus of reeler mice, lacking the extracellular matrix protein Reelin, in scrambler mice, deficient in the intracellular adaptor protein disabled1 (Dab1), which is required for the transmission of the Reelin signal into the cell, and in mutant mice lacking the Reelin receptors apolipoprotein receptor 2 (ApoER2) and/or the very low density lipoprotein receptor (VLDLR), known to transmit the Reelin signal via Dab1. By immunolabeling for the glial fibrillary acidic protein (GFAP), we show that a regular dentate radial glial scaffold fails to form in mutants deficient of Reelin, Dab1, and VLDLR and ApoER2. Mutant mice lacking only one of the Reelin receptors, VLDLR or ApoER2, display a gradual expression of the radial glial defects seen in mutants that lack both receptors. Our results suggest that Reelin signaling via ApoER2, VLDLR, and Dab1 is required for the formation of a regular radial glial scaffold in the dentate gyrus.",
author = "Weiss, {Karl Heinz} and Celine Johanssen and Albrecht Tielsch and Joachim Herz and Thomas Deller and Michael Frotscher and Eckart F{\"o}rster",
year = "2003",
language = "Deutsch",
volume = "460",
pages = "56--65",
journal = "J COMP NEUROL",
issn = "0021-9967",
publisher = "Wiley",
number = "1",

}

RIS

TY - JOUR

T1 - Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice.

AU - Weiss, Karl Heinz

AU - Johanssen, Celine

AU - Tielsch, Albrecht

AU - Herz, Joachim

AU - Deller, Thomas

AU - Frotscher, Michael

AU - Förster, Eckart

PY - 2003

Y1 - 2003

N2 - We studied the postnatal development of the radial glial scaffold in the dentate gyrus of reeler mice, lacking the extracellular matrix protein Reelin, in scrambler mice, deficient in the intracellular adaptor protein disabled1 (Dab1), which is required for the transmission of the Reelin signal into the cell, and in mutant mice lacking the Reelin receptors apolipoprotein receptor 2 (ApoER2) and/or the very low density lipoprotein receptor (VLDLR), known to transmit the Reelin signal via Dab1. By immunolabeling for the glial fibrillary acidic protein (GFAP), we show that a regular dentate radial glial scaffold fails to form in mutants deficient of Reelin, Dab1, and VLDLR and ApoER2. Mutant mice lacking only one of the Reelin receptors, VLDLR or ApoER2, display a gradual expression of the radial glial defects seen in mutants that lack both receptors. Our results suggest that Reelin signaling via ApoER2, VLDLR, and Dab1 is required for the formation of a regular radial glial scaffold in the dentate gyrus.

AB - We studied the postnatal development of the radial glial scaffold in the dentate gyrus of reeler mice, lacking the extracellular matrix protein Reelin, in scrambler mice, deficient in the intracellular adaptor protein disabled1 (Dab1), which is required for the transmission of the Reelin signal into the cell, and in mutant mice lacking the Reelin receptors apolipoprotein receptor 2 (ApoER2) and/or the very low density lipoprotein receptor (VLDLR), known to transmit the Reelin signal via Dab1. By immunolabeling for the glial fibrillary acidic protein (GFAP), we show that a regular dentate radial glial scaffold fails to form in mutants deficient of Reelin, Dab1, and VLDLR and ApoER2. Mutant mice lacking only one of the Reelin receptors, VLDLR or ApoER2, display a gradual expression of the radial glial defects seen in mutants that lack both receptors. Our results suggest that Reelin signaling via ApoER2, VLDLR, and Dab1 is required for the formation of a regular radial glial scaffold in the dentate gyrus.

M3 - SCORING: Zeitschriftenaufsatz

VL - 460

SP - 56

EP - 65

JO - J COMP NEUROL

JF - J COMP NEUROL

SN - 0021-9967

IS - 1

M1 - 1

ER -