ArticleLearning & memory (Cold Spring Harbor, N.Y.)2008
Preservation of long-term memory and synaptic plasticity despite short-term impairments in the Tc1 mouse model of Down syndrome.
Article in Learning & memory (Cold Spring Harbor, N.Y.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
51 citing papers in PubMed, 99 citations in OpenAlex.
- FORTIS: a live-cell assay to monitor AMPA receptors using pH-sensitive fluorescence tags.Translational psychiatry · 2021Article
- A Multivariate Assessment of Age-Related Cognitive Impairment inFrontiers in integrative neuroscience · 2021Article
- Inositol hexakisphosphate kinase-1 is a key mediator of prepulse inhibition and short-term fear memory.Molecular brain · 2020Article
- Loss of Function of Phosphodiesterase 11A4 Shows that Recent and Remote Long-Term Memories Can Be Uncoupled.Current biology : CB · 2019Article
- Gene expression dysregulation domains are not a specific feature of Down syndrome.Nature communications · 2019Article
- OLIG2 Drives Abnormal Neurodevelopmental Phenotypes in Human iPSC-Based Organoid and Chimeric Mouse Models of Down Syndrome.Cell stem cell · 2019Article
- Human Models Are Needed for Studying Human Neurodevelopmental Disorders.American journal of human genetics · 2018Review
- Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP.Brain : a journal of neurology · 2018Article
- Article
- In vivo and ex vivo analyses of amyloid toxicity in the Tc1 mouse model of Down syndrome.Journal of psychopharmacology (Oxford, England) · 2018Article
- A third copy of the Down syndrome cell adhesion molecule (Dscam) causes synaptic and locomotor dysfunction in Drosophila.Neurobiology of disease · 2018Article
- RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome.Frontiers in cellular neuroscience · 2018Article
- Mouse-based genetic modeling and analysis of Down syndrome.British medical bulletin · 2016Review
- Tc1 mouse model of trisomy-21 dissociates properties of short- and long-term recognition memory.Neurobiology of learning and memory · 2016Article
- Visual recognition memory: a view from V1.Current opinion in neurobiology · 2015Review
- Abnormally increased surface expression of AMPA receptors in the cerebellum, cortex and striatum of Cln3(-/-) mice.Neuroscience letters · 2015Article
- Involvement of Potassium and Cation Channels in Hippocampal Abnormalities of Embryonic Ts65Dn and Tc1 Trisomic Mice.EBioMedicine · 2015Article
- Hippocampal circuit dysfunction in the Tc1 mouse model of Down syndrome.Nature neuroscience · 2015Article
- Sleep-like behavior and 24-h rhythm disruption in the Tc1 mouse model of Down syndrome.Genes, brain, and behavior · 2015Article
- Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.Drug design, development and therapy · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Down syndrome (DS) is a genetic disorder arising from the presence of a third copy of the human chromosome 21 (Hsa21). Recently, O'Doherty and colleagues in an earlier study generated a new genetic mouse model of DS (Tc1) that carries an almost complete Hsa21. Since DS is the most common genetic cause of mental retardation, we have undertaken a detailed analysis of cognitive function and synaptic plasticity in Tc1 mice. Here we show that Tc1 mice have impaired spatial working memory (WM) but spared long-term spatial reference memory (RM) in the Morris watermaze. Similarly, Tc1 mice are selectively impaired in short-term memory (STM) but have intact long-term memory (LTM) in the novel object recognition task. The pattern of impaired STM and normal LTM is paralleled by a corresponding phenotype in long-term potentiation (LTP). Freely-moving Tc1 mice exhibit reduced LTP 1 h after induction but normal maintenance over days in the dentate gyrus of the hippocampal formation. Biochemical analysis revealed a reduction in membrane surface expression of the AMPAR (alpha-amino-3-hydroxy-5-methyl-4-propionic acid receptor) subunit GluR1 in the hippocampus of Tc1 mice, suggesting a potential mechanism for the impairment in early LTP. Our observations also provide further evidence that STM and LTM for hippocampus-dependent tasks are subserved by parallel processing streams.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.