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Cited by 32Down syndrome and intellectual disability researchMemory and Neural MechanismsGenetics and Neurodevelopmental Disorders

Alterations of in vivo CA1 network activity in Dp(16)1Yey Down syndrome model mice

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Raveau, Matthieu, Polygalov, Denis, Boehringer, Roman, Amano, Kenji, Yamakawa, Kazuhiro, McHugh, Thomas J·2018·eLife
DOI 10.7554/elife.31543PMC PMC5841929
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Abstract

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.

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  • Recent studies indicate an increased ratio of inhibitory to excitatory neurons in the cortex and hippocampus in Dp16 mice that is associated with deficits in learning, memory, and motor function.

    “recent studies that indicate an increased ratio of inhibitory to excitatory neurons in the cortex and hippocampus in Dp16 mice that is associated with deficits in learning, memory, and motor function.”

    From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [87]

    The Results (CA1 interneuron density; page unavailable) report increased density of a specific inhibitory-neuron subtype in the hippocampus of Dp16 mice. The Discussion links these changes tentatively to spatial learning and memory deficits. The paper does not establish an increased inhibitory-to-excitatory neuron ratio across the cortex and hippocampus, or link that ratio to motor-function deficits. (LLM, conf=0.90)

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Cited by

Sorted by citations

Authors
Raveau, M., Polygalov, D., Boehringer, R., Amano, K., Yamakawa, K., & McHugh, T. J.
Affiliations
  • RIKEN Center for Brain Science (JP)
  • RIKEN (JP)
Corresponding author
  • Yamakawa, Kazuhiro
  • McHugh, Thomas J
ORCID
Venue
eLife
Publisher
eLife Sciences Publications, Ltd
Published
2018-02-27
Volume
7
ISSN
2050-084X (ISSN-L)
DOI
10.7554/elife.31543
PMC
PMC5841929
OpenAlex
W2788179293
Cited by
32
References
8
Citations by year
2025: 6 · 2024: 6 · 2023: 2 · 2022: 6 · 2021: 3 · 2020: 5 · 2019: 3 · 2018: 1
FWCI
2.85
Type
journal article
Language
en
Open access
Licence
Locations
  • eLife (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
RIKEN Brain Science Institute
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
Down syndrome, hippocampal CA1, pyramidal neurons, complex spikes, sharp-wave ripples, spatial coding, memory consolidation, intellectual disability, neuronal network activity
MeSH terms
Action Potentials, Animals, Disease Models, Animal, Down Syndrome, Memory, Neuropeptide Y, Mice, CA1 Region, Hippocampal

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