The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: a model of down syndrome.
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., 2007).”
From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Costa and Grybko, 2005
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Cites
A mouse model for Down syndrome exhibits learning and behaviour deficits
Reeves, R. H., Irving, N. G., Moran, T. H., Wohn, A., Kitt, C., Sisodia, S. S., Schmidt, C., Bronson, R. T., & Davisson, M. T. (1995) · Nature Genetics · doi:10.1038/ng1095-177 · Cited by 913
Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1
Costa, R. M., Federov, N. B., Kogan, J. H., Murphy, G. G., Stern, J. N. H., Ohno, M., Kucherlapati, R., Jacks, T., & Silva, A. J. (2002) · Nature · doi:10.1038/nature711 · Cited by 590
The neuropsychology of down syndrome: evidence for hippocampal dysfunction.
Pennington, B. F., Moon, J., Edgin, J., Stedron, J., & Nadel, L. (2003) · Child Development · doi:10.1111/1467-8624.00522 · Cited by 514
Kleschevnikov, A. M., Belichenko, P. V., Villar, A. J., Epstein, C. J., Malenka, R. C., & Mobley, W. C. (2004) · The Journal of Neuroscience · doi:10.1523/jneurosci.1766-04.2004 · Cited by 459
Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome
Holtzman, D. M., Santucci, D., Kilbridge, J., Chua-Couzens, J., Fontana, D. J., Daniels, S. E., Johnson, R. M., Chen, K., Sun, Y., Carlson, E., et al. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.23.13333 · Cited by 448
Strain-dependent Differences in LTP and Hippocampus-dependent Memory in Inbred MicePreprint
Nguyen, P., Abel, T. G., Kandel, E. R., & Bourtchouladze, R. (2000) · Learning & Memory · doi:10.1101/lm.7.3.170 · Cited by 242
Granholm, A., Sanders, L., & Crnic, L. S. (2000) · Experimental Neurology · doi:10.1006/exnr.1999.7289 · Cited by 237
A behavioral assessment of Ts65Dn mice: a putative Down syndrome model
Escorihuela, R. M., Fernández‐Teruel, A., Vallina, I. F., Baamonde, C., Lumbreras, M., Dierssen, M., Tobeña, A., & Flórez, J. (1995) · Neuroscience Letters · doi:10.1016/0304-3940(95)12052-6 · Cited by 234
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 · Cited by 222
Down syndrome and genetics — a case of linked histories
Patterson, D., & Costa, A. C. S. (2005) · Nature Reviews Genetics · doi:10.1038/nrg1525 · Cited by 220
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Rethinking intellectual disability from neuro- to astro-pathology.
Fernández-Blanco, Á., & Dierssen, M. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21239039 · Cited by 19
Plasticity of Synaptic Transmission in Human Stem Cell-Derived Neural Networks
Dong, Y., Xiong, M., Chen, Y., Tao, Y., Li, X., Bhattacharyya, A., & Zhang, S.-C. (2020) · iScience · doi:10.1016/j.isci.2020.100829 · Cited by 19
Metadata
- 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)
- 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
- 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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