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,...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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eLife Sciences Publications Ltd
2018-02-01
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| Series: | eLife |
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| Online Access: | https://elifesciences.org/articles/31543 |
| _version_ | 1818023997861789696 |
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| author | Matthieu Raveau Denis Polygalov Roman Boehringer Kenji Amano Kazuhiro Yamakawa Thomas J McHugh |
| author_facet | Matthieu Raveau Denis Polygalov Roman Boehringer Kenji Amano Kazuhiro Yamakawa Thomas J McHugh |
| author_sort | Matthieu Raveau |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-12-10T03:53:13Z |
| format | Article |
| id | doaj.art-297ec264c82848ca8ea0426a52cf17a2 |
| institution | Directory Open Access Journal |
| issn | 2050-084X |
| language | English |
| last_indexed | 2024-12-10T03:53:13Z |
| publishDate | 2018-02-01 |
| publisher | eLife Sciences Publications Ltd |
| record_format | Article |
| series | eLife |
| spelling | doaj.art-297ec264c82848ca8ea0426a52cf17a22022-12-22T02:03:12ZengeLife Sciences Publications LtdeLife2050-084X2018-02-01710.7554/eLife.31543Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model miceMatthieu Raveau0https://orcid.org/0000-0002-3951-3861Denis Polygalov1https://orcid.org/0000-0002-8165-5257Roman Boehringer2https://orcid.org/0000-0003-2856-3262Kenji Amano3Kazuhiro Yamakawa4Thomas J McHugh5https://orcid.org/0000-0002-1243-5189Laboratory for Neurogenetics, RIKEN, Brain Science Institute, Saitama, JapanLaboratory for Circuit and Behavioral Physiology, RIKEN, Brain Science Institute, Saitama, JapanLaboratory for Circuit and Behavioral Physiology, RIKEN, Brain Science Institute, Saitama, JapanLaboratory for Neurogenetics, RIKEN, Brain Science Institute, Saitama, JapanLaboratory for Neurogenetics, RIKEN, Brain Science Institute, Saitama, JapanLaboratory for Circuit and Behavioral Physiology, RIKEN, Brain Science Institute, Saitama, JapanDown 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.https://elifesciences.org/articles/31543hippocampusDown syndromeplace cellripples |
| spellingShingle | Matthieu Raveau Denis Polygalov Roman Boehringer Kenji Amano Kazuhiro Yamakawa Thomas J McHugh Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice eLife hippocampus Down syndrome place cell ripples |
| 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 | hippocampus Down syndrome place cell ripples |
| url | https://elifesciences.org/articles/31543 |
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