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Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro

Neuroligins (Nlgns) are postsynaptic cell adhesion molecules that form transynaptic complexes with presynaptic neurexins and regulate synapse maturation and plasticity. We studied the impact of the loss of Nlgn4 on the excitatory and inhibitory circuits in somatosensory cortical slices of juvenile m...

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Autores principales: Delattre, V., La Mendola, D., Meystre, J., Markram, H., Markram, K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3793213/
https://www.ncbi.nlm.nih.gov/pubmed/24104404
http://dx.doi.org/10.1038/srep02897
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author Delattre, V.
La Mendola, D.
Meystre, J.
Markram, H.
Markram, K.
author_facet Delattre, V.
La Mendola, D.
Meystre, J.
Markram, H.
Markram, K.
author_sort Delattre, V.
collection PubMed
description Neuroligins (Nlgns) are postsynaptic cell adhesion molecules that form transynaptic complexes with presynaptic neurexins and regulate synapse maturation and plasticity. We studied the impact of the loss of Nlgn4 on the excitatory and inhibitory circuits in somatosensory cortical slices of juvenile mice by electrically stimulating these circuits using a multi-electrode array and recording the synaptic input to single neurons using the patch-clamp technique. We detected a decreased network response to stimulation in both excitatory and inhibitory circuits of Nlgn4 knock-out animals as compared to wild-type controls, and a decreased excitation-inhibition ratio. These data indicate that Nlgn4 is involved in the regulation of excitatory and inhibitory circuits and contributes to a balanced circuit response to stimulation.
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spelling pubmed-37932132013-10-18 Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro Delattre, V. La Mendola, D. Meystre, J. Markram, H. Markram, K. Sci Rep Article Neuroligins (Nlgns) are postsynaptic cell adhesion molecules that form transynaptic complexes with presynaptic neurexins and regulate synapse maturation and plasticity. We studied the impact of the loss of Nlgn4 on the excitatory and inhibitory circuits in somatosensory cortical slices of juvenile mice by electrically stimulating these circuits using a multi-electrode array and recording the synaptic input to single neurons using the patch-clamp technique. We detected a decreased network response to stimulation in both excitatory and inhibitory circuits of Nlgn4 knock-out animals as compared to wild-type controls, and a decreased excitation-inhibition ratio. These data indicate that Nlgn4 is involved in the regulation of excitatory and inhibitory circuits and contributes to a balanced circuit response to stimulation. Nature Publishing Group 2013-10-09 /pmc/articles/PMC3793213/ /pubmed/24104404 http://dx.doi.org/10.1038/srep02897 Text en Copyright © 2013, Macmillan Publishers Limited. All rights reserved http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
spellingShingle Article
Delattre, V.
La Mendola, D.
Meystre, J.
Markram, H.
Markram, K.
Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title_full Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title_fullStr Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title_full_unstemmed Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title_short Nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
title_sort nlgn4 knockout induces network hypo-excitability in juvenile mouse somatosensory cortex in vitro
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3793213/
https://www.ncbi.nlm.nih.gov/pubmed/24104404
http://dx.doi.org/10.1038/srep02897
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