ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 198 citations in OpenAlex.
- Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.G3 (Bethesda, Md.) · 2026Article
- Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome.Brain research bulletin · 2026Article
- Cardiopulmonary and Immune Alterations in the Ts65Dn Mouse Model of Down Syndrome and Modulation by Epigallocatechin-3-Gallate-Enriched Green Tea Extract.Pharmaceutics · 2025Article
- Senescent hearts from male Ts65Dn mice exhibit preserved function but altered size and nicotinamide adenine dinucleotide pathway signaling.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Down syndrome and DYRK1A overexpression: relationships and future therapeutic directions.Frontiers in molecular neuroscience · 2024Review
- Hippocampal CA1 Pyramidal Neurons Display Sublayer and Circuitry Dependent Degenerative Expression Profiles in Aged Female Down Syndrome Mice.Journal of Alzheimer's disease : JAD · 2024Article
- Understanding the genetic mechanisms and cognitive impairments in Down syndrome: towards a holistic approach.Journal of neurology · 2024Review
- Single-nucleus RNA sequencing reveals cell type-specific transcriptome alterations of Down syndrome hippocampus using the Dp16 mouse model.Genes & genomics · 2023Article
- Volume of the thalamus and hypothalamus in the Ts1Rhr and Ms1Rhr mouse models relevant to Down syndrome.microPublication biology · 2023Article
- Sexually dimorphic DYRK1A overexpression on postnatal day 15 in the Ts65Dn mouse model of Down syndrome: Effects of pharmacological targeting on behavioral phenotypes.Pharmacology, biochemistry, and behavior · 2022Article
- Cardiovascular physiology and pathophysiology in Down syndrome.Physiological research · 2022Article
- Modeling human neurodevelopmental diseases with brain organoids.Cell regeneration (London, England) · 2022Review
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- GIRK2 Channels in Down Syndrome and Alzheimer's Disease.Current Alzheimer research · 2022Article
- Arhgap22 Disruption Leads to RAC1 Hyperactivity Affecting Hippocampal Glutamatergic Synapses and Cognition in Mice.Molecular neurobiology · 2021Article
- Role of DSCAM in the Development of Neural Control of Movement and Locomotion.International journal of molecular sciences · 2021Review
- Multi-influential genetic interactions alter behaviour and cognition through six main biological cascades in Down syndrome mouse models.Human molecular genetics · 2021Article
- Astrocytes in Down Syndrome Across the Lifespan.Frontiers in cellular neuroscience · 2021Review
- Article
- Genetic and epigenetic pathways in Down syndrome: Insights to the brain and immune system from humans and mouse models.Progress in brain research · 2020Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Down syndrome (DS) can be modeled in mice segmentally trisomic for mouse chromosome 16. Ts65Dn and Ts1Cje mouse models have been used to study DS neurobiological phenotypes including changes in cognitive ability, induction of long-term potentiation (LTP) in the fascia dentata (FD), the density and size of dendritic spines, and the structure of synapses. To explore the genetic basis for these phenotypes, we examined Ts1Rhr mice that are trisomic for a small subset of the genes triplicated in Ts65Dn and Ts1Cje mice. The 33 trisomic genes in Ts1Rhr represent a "DS critical region" that was once predicted to be sufficient to produce most DS phenotypes. We discovered significant alterations in an open field test, a novel object recognition test and in a T-maze task. As in Ts65Dn and Ts1Cje mice, LTP in FD of Ts1Rhr could be induced only after blocking GABA(A)-dependent inhibitory neurotransmission. In addition, widespread enlargement of dendritic spines and decreased density of spines in FD were preserved in Ts1Rhr. Twenty of 48 phenotypes showed significant differences between Ts1Rhr and 2N controls. We conclude that important neurobiological phenotypes characteristic of DS are conserved in Ts1Rhr mice. The data support the view that biologically significant trisomic phenotypes occur because of dosage effects of genes in the Ts1Rhr trisomic segment and that increased dosage is sufficient to produce these changes. The stage is now set for studies to decipher the gene(s) that play a conspicuous role in creating these phenotypes.
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