Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndrome

Siarey, R.J.; Stoll, J.; Rapoport, S.I.; Galdzicki, Z.

doi:10.1016/s0028-3908(97)00157-3

Cited by 222Down syndrome and intellectual disability researchNeuroscience and Neuropharmacology ResearchGenetics and Neurodevelopmental Disorders

Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndrome

Siarey, R.J., Stoll, J., Rapoport, S.I., Galdzicki, Z.·1997·Neuropharmacology

DOI 10.1016/s0028-3908(97)00157-3

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Abstract

We investigated the phenomenon of long-term potentiation (LTP) in a genetic model of Down Syndrome, the segmental trisomy mouse (Ts65Dn). Ts65Dn mice survive to adulthood and have an extra chromosome that contains a segment of chromosome 16 homologous to human chromosome 21. In this study, field excitatory postsynaptic potentials (fEPSP) were recorded from the CA1 area of in vitro hippocampal slices from diploid and Ts65Dn mice, and LTP was induced by a single tetanizing pulse train (1 sec in duration) at 100 Hz. The hippocampus from both young (2 months) and older (9 months) Ts65Dn mice had a reduced LTP over a period of 60 min compared with LTP in age-matched controls. This finding may explain the reported behavioral and learning impairments in Ts65Dn mice; it suggests that this mouse model can be used to study the role of altered synaptic plasticity in mental retardation of Down Syndrome.

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Findings from mouse models of Down syndrome, particularly the Ts65Dn model, show reduced long-term potentiation and increased long-term depression, reflecting the relative strengthening and weakening, respectively, of individual synapses.
“This suggestion is largely driven by findings from mouse models of DS, particularly the Ts65Dn model, in which patch clamp electrophysiology analyses reveal reduced long-term potentiation (LTP) and increased long-term depression (LTD), reflecting the relative strengthening and weakening, respectively, of individual synapses123–126.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [123]

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Authors: Siarey, R. J., Stoll, J., Rapoport, S. I., & Galdzicki, Z.
Affiliations: National Institutes of Health (US)
Texas Tech University (US)
Corresponding author: Siarey, R.J.
Galdzicki, Z.
ORCID: Stoll, J.
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 1997-11
Volume: 36
Issue: 11-12
Pages: 1549-1554
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/s0028-3908(97)00157-3
OpenAlex: W2019373887
Cited by: 222
References: 37
Citations by year: 2026: 3 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 7 · 2020: 8 · 2019: 8 · 2018: 7 · 2017: 9 · 2016: 5 · 2015: 9 · 2014: 6 · 2013: 11 · 2012: 20
FWCI: 6.47
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords: long-term potentiation, Ts65Dn mouse model, Down syndrome, hippocampal CA1, field excitatory postsynaptic potentials, synaptic plasticity, age-related decline, learning disabilities, intellectual disability, chromosome 21
MeSH terms: Aging, Animals, Diploidy, Down Syndrome, Electric Stimulation, Electrophysiology, Female, Karyotyping, Male, Mice, Neurologic Mutants, Trisomy, Long-Term Potentiation, Mice, In Vitro Techniques

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Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndrome

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