Deficits of neuronal density in CA1 and synaptic density in the dentate gyrus, CA3 and CA1, in a mouse model of Down syndrome
Abstract
Ts65Dn mice are partially trisomic for the distal region of MMU16, which is homologous with the obligate segment of HSA21 triplicated in Down syndrome (DS). Ts65Dn mice are impaired in learning tasks that require an intact hippocampus. In order to investigate the neural basis of these deficits in this mouse model of Down syndrome, quantitative light and electron microscopy were used to compare the volume densities of neurons and synapses in the hippocampus of adult Ts65Dn (n=4) and diploid mice (n=4). Neuron density was significantly lower in the CA1 of Ts65Dn compared to diploid mice (p<0.01). Total synapse density was significantly lower in the dentate gyrus (DG; p<0.001), CA3 (p<0.05) and CA1 (p<0.001) of Ts65Dn compared to diploid mice. The synapse-to-neuron ratio was significantly lower in the DG (p<0.001), CA3 (p<0.01) and CA1 (p<0.001) of Ts65Dn compared to diploid mice. When the data were broken down by synapse type, asymmetric synapse density was found to be significantly lower in the DG (p<0.001), CA3 (p<0.05) and CA1 (p<0.001) of Ts65Dn compared to diploid mice, while such a difference in symmetric synapse density was only present in the DG (p<0.01). The asymmetric synapse-to-neuron ratio was significantly lower in the DG (p<0.001), CA3 (p<0.01) and CA1 (p<0.001) of Ts65Dn compared to diploid mice, but there were no such significant differences in symmetric synapse-to-neuron ratios. These results suggest that impaired synaptic connectivity in the hippocampus of Ts6…
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The reduced capacity for long-term potentiation in Ts65Dn animals is driven by increased GABAergic neurotransmission, and pharmacological reduction of GABAergic neurotransmission is sufficient to rescue this long-term potentiation phenotype.
“The reduced capacity for LTP is driven by increased GABAergic neurotransmission in these animals, and pharmacological reduction of GABAergic neurotransmission is sufficient to rescue this LTP phenotype127–129.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [127]
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References 74 · Cited by 126
- Authors
- Ayberk Kurt, M., Ilker Kafa, M., Dierssen, M., & Ceri Davies, D.
- Affiliations
- Centre for Genomic Regulation (ES)
- ORCID
- Dierssen, Mara
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2004-10
- Volume
- 1022
- Issue
- 1-2
- Pages
- 101-109
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2083883439
- Cited by
- 126
- References
- 74
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 7 · 2018: 7 · 2017: 11 · 2016: 3 · 2015: 6 · 2014: 5 · 2013: 3 · 2012: 14
- FWCI
- 5.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Bursa Uludag University - AVESIS (submittedVersion)
- Funders
- Bursa Uludağ Üniversitesi
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Down syndrome, Ts65Dn mouse model, trisomy 16, hippocampus, neuronal density, synaptic density, asymmetric synapses, symmetric synapses, CA1, dentate gyrus, CA3, synaptic connectivity, learning deficits, cognitive impairment
- MeSH terms
- Animals, Cell Count, Diploidy, Disease Models, Animal, Down Syndrome, Hippocampus, Male, Neurons, Synapses, Trisomy, Dentate Gyrus, Microscopy, Electron, Transmission, Mice
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