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Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines

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Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines. / Köster, Jan-Dietrich; Leggewie, Birthe; Blechner, Christine; Brandt, Nicola; Fester, Lars; Rune, Gabriele; Schweizer, Michaela; Kindler, Stefan; Windhorst, Sabine.

In: CELL SIGNAL, Vol. 28, No. 1, 01.2016, p. 83-90.

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

Harvard

Köster, J-D, Leggewie, B, Blechner, C, Brandt, N, Fester, L, Rune, G, Schweizer, M, Kindler, S & Windhorst, S 2016, 'Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines', CELL SIGNAL, vol. 28, no. 1, pp. 83-90. https://doi.org/10.1016/j.cellsig.2015.10.016

APA

Köster, J-D., Leggewie, B., Blechner, C., Brandt, N., Fester, L., Rune, G., Schweizer, M., Kindler, S., & Windhorst, S. (2016). Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines. CELL SIGNAL, 28(1), 83-90. https://doi.org/10.1016/j.cellsig.2015.10.016

Vancouver

Köster J-D, Leggewie B, Blechner C, Brandt N, Fester L, Rune G et al. Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines. CELL SIGNAL. 2016 Jan;28(1):83-90. https://doi.org/10.1016/j.cellsig.2015.10.016

Bibtex

@article{c3395ef44cfe4b96aa1e4083ed2186c2,
title = "Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines",
abstract = "Long-lasting synaptic plasticity is often accompanied by morphological changes as well as formation and/or loss of dendritic spines. Since the spine cytoskeleton mainly consists of actin filaments, morphological changes are primarily controlled by actin binding proteins (ABPs). Inositol-1,4,5-trisphosphate-3-kinase-A (ITPKA) is a neuron-specific, actin bundling protein concentrated at dendritic spines. Here, we demonstrate that ITPKA depletion in mice increases the number of hippocampal spine-synapses while reducing average spine length. By employing actin to ABP ratios similar to those occurring at post synaptic densities, in addition to cross-linking actin filaments, ITPKA strongly inhibits Arp2/3-complex induced actin filament branching by displacing the complex from F-actin. In summary, our data show that in vivo ITPKA negatively regulates formation and/or maintenance of synaptic contacts in the mammalian brain. On the molecular level this effect appears to result from the ITPKA-mediated inhibition of Arp2/3-complex F-actin branching activity.",
author = "Jan-Dietrich K{\"o}ster and Birthe Leggewie and Christine Blechner and Nicola Brandt and Lars Fester and Gabriele Rune and Michaela Schweizer and Stefan Kindler and Sabine Windhorst",
note = "Copyright {\textcopyright} 2015 Elsevier Inc. All rights reserved.",
year = "2016",
month = jan,
doi = "10.1016/j.cellsig.2015.10.016",
language = "English",
volume = "28",
pages = "83--90",
journal = "CELL SIGNAL",
issn = "0898-6568",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Inositol-1,4,5-trisphosphate-3-kinase-A controls morphology of hippocampal dendritic spines

AU - Köster, Jan-Dietrich

AU - Leggewie, Birthe

AU - Blechner, Christine

AU - Brandt, Nicola

AU - Fester, Lars

AU - Rune, Gabriele

AU - Schweizer, Michaela

AU - Kindler, Stefan

AU - Windhorst, Sabine

N1 - Copyright © 2015 Elsevier Inc. All rights reserved.

PY - 2016/1

Y1 - 2016/1

N2 - Long-lasting synaptic plasticity is often accompanied by morphological changes as well as formation and/or loss of dendritic spines. Since the spine cytoskeleton mainly consists of actin filaments, morphological changes are primarily controlled by actin binding proteins (ABPs). Inositol-1,4,5-trisphosphate-3-kinase-A (ITPKA) is a neuron-specific, actin bundling protein concentrated at dendritic spines. Here, we demonstrate that ITPKA depletion in mice increases the number of hippocampal spine-synapses while reducing average spine length. By employing actin to ABP ratios similar to those occurring at post synaptic densities, in addition to cross-linking actin filaments, ITPKA strongly inhibits Arp2/3-complex induced actin filament branching by displacing the complex from F-actin. In summary, our data show that in vivo ITPKA negatively regulates formation and/or maintenance of synaptic contacts in the mammalian brain. On the molecular level this effect appears to result from the ITPKA-mediated inhibition of Arp2/3-complex F-actin branching activity.

AB - Long-lasting synaptic plasticity is often accompanied by morphological changes as well as formation and/or loss of dendritic spines. Since the spine cytoskeleton mainly consists of actin filaments, morphological changes are primarily controlled by actin binding proteins (ABPs). Inositol-1,4,5-trisphosphate-3-kinase-A (ITPKA) is a neuron-specific, actin bundling protein concentrated at dendritic spines. Here, we demonstrate that ITPKA depletion in mice increases the number of hippocampal spine-synapses while reducing average spine length. By employing actin to ABP ratios similar to those occurring at post synaptic densities, in addition to cross-linking actin filaments, ITPKA strongly inhibits Arp2/3-complex induced actin filament branching by displacing the complex from F-actin. In summary, our data show that in vivo ITPKA negatively regulates formation and/or maintenance of synaptic contacts in the mammalian brain. On the molecular level this effect appears to result from the ITPKA-mediated inhibition of Arp2/3-complex F-actin branching activity.

U2 - 10.1016/j.cellsig.2015.10.016

DO - 10.1016/j.cellsig.2015.10.016

M3 - SCORING: Journal article

C2 - 26519023

VL - 28

SP - 83

EP - 90

JO - CELL SIGNAL

JF - CELL SIGNAL

SN - 0898-6568

IS - 1

ER -