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Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice
Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models,...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
eLife Sciences Publications, Ltd
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841929/ https://www.ncbi.nlm.nih.gov/pubmed/29485402 http://dx.doi.org/10.7554/eLife.31543 |
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author | Raveau, Matthieu Polygalov, Denis Boehringer, Roman Amano, Kenji Yamakawa, Kazuhiro McHugh, Thomas J |
author_facet | Raveau, Matthieu Polygalov, Denis Boehringer, Roman Amano, Kenji Yamakawa, Kazuhiro McHugh, Thomas J |
author_sort | Raveau, Matthieu |
collection | PubMed |
description | Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models, most studies have relied on in vitro measures. Here, using in vivo recording in the Dp(16)1Yey model, we find alterations in the organization of spiking of hippocampal CA1 pyramidal neurons, including deficits in the generation of complex spikes. These changes lead to poorer spatial coding during exploration and less coordinated activity during sharp-wave ripples, events involved in memory consolidation. Further, the density of CA1 inhibitory neurons expressing neuropeptide Y, a population key for the generation of pyramidal cell bursts, were significantly increased in Dp(16)1Yey mice. Our data refine the ‘over-suppression’ theory of Down syndrome pathophysiology and suggest specific neuronal subtypes involved in hippocampal dysfunction in these model mice. |
format | Online Article Text |
id | pubmed-5841929 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | eLife Sciences Publications, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-58419292018-03-09 Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice Raveau, Matthieu Polygalov, Denis Boehringer, Roman Amano, Kenji Yamakawa, Kazuhiro McHugh, Thomas J eLife Neuroscience Down syndrome, the leading genetic cause of intellectual disability, results from an extra-copy of chromosome 21. Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models, most studies have relied on in vitro measures. Here, using in vivo recording in the Dp(16)1Yey model, we find alterations in the organization of spiking of hippocampal CA1 pyramidal neurons, including deficits in the generation of complex spikes. These changes lead to poorer spatial coding during exploration and less coordinated activity during sharp-wave ripples, events involved in memory consolidation. Further, the density of CA1 inhibitory neurons expressing neuropeptide Y, a population key for the generation of pyramidal cell bursts, were significantly increased in Dp(16)1Yey mice. Our data refine the ‘over-suppression’ theory of Down syndrome pathophysiology and suggest specific neuronal subtypes involved in hippocampal dysfunction in these model mice. eLife Sciences Publications, Ltd 2018-02-27 /pmc/articles/PMC5841929/ /pubmed/29485402 http://dx.doi.org/10.7554/eLife.31543 Text en © 2018, Raveau et al http://creativecommons.org/licenses/by/4.0/ http://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited. |
spellingShingle | Neuroscience Raveau, Matthieu Polygalov, Denis Boehringer, Roman Amano, Kenji Yamakawa, Kazuhiro McHugh, Thomas J Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title | Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title_full | Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title_fullStr | Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title_full_unstemmed | Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title_short | Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice |
title_sort | alterations of in vivo ca1 network activity in dp(16)1yey down syndrome model mice |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5841929/ https://www.ncbi.nlm.nih.gov/pubmed/29485402 http://dx.doi.org/10.7554/eLife.31543 |
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