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Role for Reelin in stabilizing cortical architecture.

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Role for Reelin in stabilizing cortical architecture. / Frotscher, Michael.

In: TRENDS NEUROSCI, Vol. 33, No. 9, 9, 2010, p. 407-414.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Frotscher, M 2010, 'Role for Reelin in stabilizing cortical architecture.', TRENDS NEUROSCI, vol. 33, no. 9, 9, pp. 407-414. <http://www.ncbi.nlm.nih.gov/pubmed/20598379?dopt=Citation>

APA

Frotscher, M. (2010). Role for Reelin in stabilizing cortical architecture. TRENDS NEUROSCI, 33(9), 407-414. [9]. http://www.ncbi.nlm.nih.gov/pubmed/20598379?dopt=Citation

Vancouver

Frotscher M. Role for Reelin in stabilizing cortical architecture. TRENDS NEUROSCI. 2010;33(9):407-414. 9.

Bibtex

@article{c868bc23e32b42a2b5f1dfe9f8735bc0,
title = "Role for Reelin in stabilizing cortical architecture.",
abstract = "Reelin controls the migration of neurons and layer formation during brain development. However, recent studies have shown that disrupting Reelin function in the adult hippocampus induces repositioning of fully differentiated neurons, suggesting a stabilizing effect of Reelin on mature neuronal circuitry. Indeed, Reelin was recently found to stabilize the actin cytoskeleton by inducing cofilin phosphorylation. When unphosphorylated, cofilin acts as an actin-depolymerizing protein that promotes the disassembly of F-actin. Here, a novel hypothesis is proposed whereby decreased Reelin expression in the mature brain causes destabilization of neurons and their processes, leading to aberrant plasticity and aberrant wiring of brain circuitry. This has implications for brain disorders, such as epilepsy and schizophrenia, in which deficiencies in Reelin expression occur.",
keywords = "Animals, Humans, Signal Transduction physiology, Cerebral Cortex cytology, Cell Movement physiology, Neuronal Plasticity physiology, Neurons cytology, Cell Adhesion Molecules, Neuronal genetics, Extracellular Matrix Proteins genetics, Nerve Tissue Proteins genetics, Serine Endopeptidases genetics, Epilepsy metabolism, Actin Depolymerizing Factors metabolism, Actins metabolism, Cytoskeleton metabolism, Receptors, Notch metabolism, Schizophrenia metabolism, Animals, Humans, Signal Transduction physiology, Cerebral Cortex cytology, Cell Movement physiology, Neuronal Plasticity physiology, Neurons cytology, Cell Adhesion Molecules, Neuronal genetics, Extracellular Matrix Proteins genetics, Nerve Tissue Proteins genetics, Serine Endopeptidases genetics, Epilepsy metabolism, Actin Depolymerizing Factors metabolism, Actins metabolism, Cytoskeleton metabolism, Receptors, Notch metabolism, Schizophrenia metabolism",
author = "Michael Frotscher",
year = "2010",
language = "Deutsch",
volume = "33",
pages = "407--414",
journal = "TRENDS NEUROSCI",
issn = "0166-2236",
publisher = "Elsevier Limited",
number = "9",

}

RIS

TY - JOUR

T1 - Role for Reelin in stabilizing cortical architecture.

AU - Frotscher, Michael

PY - 2010

Y1 - 2010

N2 - Reelin controls the migration of neurons and layer formation during brain development. However, recent studies have shown that disrupting Reelin function in the adult hippocampus induces repositioning of fully differentiated neurons, suggesting a stabilizing effect of Reelin on mature neuronal circuitry. Indeed, Reelin was recently found to stabilize the actin cytoskeleton by inducing cofilin phosphorylation. When unphosphorylated, cofilin acts as an actin-depolymerizing protein that promotes the disassembly of F-actin. Here, a novel hypothesis is proposed whereby decreased Reelin expression in the mature brain causes destabilization of neurons and their processes, leading to aberrant plasticity and aberrant wiring of brain circuitry. This has implications for brain disorders, such as epilepsy and schizophrenia, in which deficiencies in Reelin expression occur.

AB - Reelin controls the migration of neurons and layer formation during brain development. However, recent studies have shown that disrupting Reelin function in the adult hippocampus induces repositioning of fully differentiated neurons, suggesting a stabilizing effect of Reelin on mature neuronal circuitry. Indeed, Reelin was recently found to stabilize the actin cytoskeleton by inducing cofilin phosphorylation. When unphosphorylated, cofilin acts as an actin-depolymerizing protein that promotes the disassembly of F-actin. Here, a novel hypothesis is proposed whereby decreased Reelin expression in the mature brain causes destabilization of neurons and their processes, leading to aberrant plasticity and aberrant wiring of brain circuitry. This has implications for brain disorders, such as epilepsy and schizophrenia, in which deficiencies in Reelin expression occur.

KW - Animals

KW - Humans

KW - Signal Transduction physiology

KW - Cerebral Cortex cytology

KW - Cell Movement physiology

KW - Neuronal Plasticity physiology

KW - Neurons cytology

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Extracellular Matrix Proteins genetics

KW - Nerve Tissue Proteins genetics

KW - Serine Endopeptidases genetics

KW - Epilepsy metabolism

KW - Actin Depolymerizing Factors metabolism

KW - Actins metabolism

KW - Cytoskeleton metabolism

KW - Receptors, Notch metabolism

KW - Schizophrenia metabolism

KW - Animals

KW - Humans

KW - Signal Transduction physiology

KW - Cerebral Cortex cytology

KW - Cell Movement physiology

KW - Neuronal Plasticity physiology

KW - Neurons cytology

KW - Cell Adhesion Molecules, Neuronal genetics

KW - Extracellular Matrix Proteins genetics

KW - Nerve Tissue Proteins genetics

KW - Serine Endopeptidases genetics

KW - Epilepsy metabolism

KW - Actin Depolymerizing Factors metabolism

KW - Actins metabolism

KW - Cytoskeleton metabolism

KW - Receptors, Notch metabolism

KW - Schizophrenia metabolism

M3 - SCORING: Zeitschriftenaufsatz

VL - 33

SP - 407

EP - 414

JO - TRENDS NEUROSCI

JF - TRENDS NEUROSCI

SN - 0166-2236

IS - 9

M1 - 9

ER -