Cited by 174Down syndrome and intellectual disability researchNeuroscience and Neuropharmacology ResearchMemory and Neural Mechanisms

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Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: a model of down syndrome.

Costa, Alberto C.S., Grybko, Michael J.·2005·Neuroscience Letters

DOI 10.1016/j.neulet.2005.03.031

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Abstract

Down syndrome (DS) is the most common genetically defined cause of intellectual disabilities. Both hippocampal function and volume seem to be disproportionally reduced in individuals with DS and in at least one aneuploid murine model of DS, the Ts65Dn mouse. Two previous studies by one research group have reported deficits in long-term potentiation (LTP) induced by in vitro high-frequency stimulation (HFS) of hippocampal CA1 synapses of adult Ts65Dn mice. Here, we report on the results of our own investigation on LTP in Ts65Dn mice. This study was designed to confirm the previous findings and possibly shed some light onto potential mechanisms underlying the reported deficit in this important form of long-term synaptic plasticity in a mouse model of DS. LTP was induced in area CA1 with either theta burst stimulation (TBS) or HFS. Contrary to the previous reports, our results showed no significant difference in HFS-induced LTP between Ts65Dn and euploid littermate mice. We have found, however, a significant reduction of the amount of TBS-induced LTP in Ts65Dn mice compared to euploid controls. Because this specific LTP deficit can be rescued by bath application of picrotoxin (10 microM), we hypothesize that an increase in GABA(A)-mediated inhibition or in plasticity of the inhibitory circuitry in Ts65Dn mice may underlie the observed deficits. However, future experiments to examine the state of hippocampus CA1 GABAergic inhibition in Ts65Dn mice will be necessary to further exp…

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“A seminal study in the field found failure of induction of long-term potentiation (LTP) in the Ts65Dn hippocampus due to excessive GABA-mediated inhibition and a wide array of following studies have confirmed this finding (Siarey et al., 1997, 1999; Kleschevnikov et al., 2004; Costa and Grybko, 2005; Fernandez et al.,…”
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Authors: Costa, A. C. S., & Grybko, M. J.
Affiliations: University of Denver (US)
Corresponding author: Costa, Alberto C.S.
ORCID: Costa, Alberto C.S.
Venue: Neuroscience Letters
Publisher: Elsevier BV
Published: 2005-07
Volume: 382
Issue: 3
Pages: 317-322
ISSN: 0304-3940 (ISSN-L)
DOI: 10.1016/j.neulet.2005.03.031
OpenAlex: W2082869264
Cited by: 174
References: 25
Citations by year: 2026: 2 · 2025: 8 · 2024: 3 · 2023: 3 · 2022: 5 · 2021: 13 · 2020: 7 · 2019: 11 · 2018: 8 · 2017: 9 · 2016: 6 · 2015: 7 · 2014: 7 · 2013: 12 · 2012: 14
FWCI: 7.69
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuroscience Letters (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD037424, R01HD037113, HD-24605, HD37424, P01HD024605, HD37113)
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 › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords: Down syndrome, Ts65Dn mouse model, hippocampal CA1, long-term potentiation, theta burst stimulation, high-frequency stimulation, picrotoxin, GABAA inhibition, synaptic plasticity, intellectual disability, aneuploidy
MeSH terms: Animals, Disease Models, Animal, Down Syndrome, Electric Stimulation, Hippocampus, Male, Synaptic Transmission, Organ Culture Techniques, Picrotoxin, Long-Term Potentiation, GABA Antagonists, Excitatory Postsynaptic Potentials, Mice

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Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: a model of down syndrome.

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