ArticleNeurochemical research2015
Altered distribution of hippocampal interneurons in the murine Down Syndrome model Ts65Dn.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 46 citations in OpenAlex.
- Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex.Science (New York, N.Y.) · 2026Article
- Increased dendritic inhibition of dentate gyrus granule cells in a mouse model of Down syndrome.Frontiers in cellular neuroscience · 2026Article
- Neuronal oscillations in cognition: Down syndrome as a model of mouse to human translation.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2025Review
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity, and memory deficits in Down syndrome.Molecular psychiatry · 2024Article
- The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity and memory deficits in Down syndrome.Research square · 2023Article
- Hyper-Rigid Phasic Organization of Hippocampal Activity But Normal Spatial Properties of CA1 Place Cells in the Ts65Dn Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Neurodevelopment in Down syndrome: Concordance in humans and models.Frontiers in cellular neuroscience · 2022Review
- The Challenging Pathway of Treatment for Neurogenesis Impairment in Down Syndrome: Achievements and Perspectives.Frontiers in cellular neuroscience · 2022Review
- Multi-influential genetic interactions alter behaviour and cognition through six main biological cascades in Down syndrome mouse models.Human molecular genetics · 2021Article
- Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down syndrome.Neuronal signaling · 2021Review
- Article
- Interneuron deficits in neurodevelopmental disorders: Implications for disease pathology and interneuron-based therapies.European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society · 2020Review
- Spatiotemporal development of spinal neuronal and glial populations in the Ts65Dn mouse model of Down syndrome.Journal of neurodevelopmental disorders · 2019Article
- Unbalanced dendritic inhibition of CA1 neurons drives spatial-memory deficits in the Ts2Cje Down syndrome model.Nature communications · 2019Article
- OLIG2 Drives Abnormal Neurodevelopmental Phenotypes in Human iPSC-Based Organoid and Chimeric Mouse Models of Down Syndrome.Cell stem cell · 2019Article
- Dynamic Causal Modeling of the Relationship between Cognition and Theta-alpha Oscillations in Adults with Down Syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Prenatal treatment with EGCG enriched green tea extract rescues GAD67 related developmental and cognitive defects in Down syndrome mouse models.Scientific reports · 2019Article
- Article
- The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome.Frontiers in cellular neuroscience · 2017Review
- Disruption of ArhGAP15 results in hyperactive Rac1, affects the architecture and function of hippocampal inhibitory neurons and causes cognitive deficits.Scientific reports · 2016Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down Syndrome, with an incidence of one in 800 live births, is the most common genetic alteration producing intellectual disability. We have used the Ts65Dn model, that mimics some of the alterations observed in Down Syndrome. This genetic alteration induces an imbalance between excitation and inhibition that has been suggested as responsible for the cognitive impairment present in this syndrome. The hippocampus has a crucial role in memory processing and is an important area to analyze this imbalance. In this report we have analysed, in the hippocampus of Ts65Dn mice, the expression of synaptic markers: synaptophysin, vesicular glutamate transporter-1 and isoform 67 of the glutamic acid decarboxylase; and of different subtypes of inhibitory neurons (Calbindin D-28k, parvalbumin, calretinin, NPY, CCK, VIP and somatostatin). We have observed alterations in the inhibitory neuropil in the hippocampus of Ts65Dn mice. There was an excess of inhibitory puncta and a reduction of the excitatory ones. In agreement with this observation, we have observed an increase in the number of inhibitory neurons in CA1 and CA3, mainly interneurons expressing calbindin, calretinin, NPY and VIP, whereas parvalbumin cell numbers were not affected. These alterations in the number of interneurons, but especially the alterations in the proportion of the different types, may influence the normal function of inhibitory circuits and underlie the cognitive deficits observed in DS.
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