ArticleNature communications2019
Unbalanced dendritic inhibition of CA1 neurons drives spatial-memory deficits in the Ts2Cje Down syndrome model.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 33 citations in OpenAlex.
- SP3-Mediated Transcriptional Activation of GRIK1 is Involved in Alzheimer's Disease-Induced Cognitive Decline by Inducing Inflammasome Activation in Microglia.Neuromolecular medicine · 2025Article
- Single-nucleus RNA sequencing-based construction of a hippocampal neuron atlas in mice with epileptic cognitive impairment.iScience · 2024Article
- 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
- Cell type characterization of spatiotemporal gene co-expression modules in Down syndrome brain.iScience · 2023Article
- From neurodevelopment to neurodegeneration: utilizing human stem cell models to gain insight into Down syndrome.Frontiers in genetics · 2023Review
- New insights into the regulation ofFrontiers in neuroscience · 2022Article
- Downregulation of kainate receptors regulating GABAergic transmission in amygdala after early life stress is associated with anxiety-like behavior in rodents.Translational psychiatry · 2021Article
- Generation of mitochondrial reactive oxygen species is controlled by ATPase inhibitory factor 1 and regulates cognition.PLoS biology · 2021Article
- Partial Monosomy 21 Mirrors Gene Expression of Trisomy 21 in a Patient-Derived Neuroepithelial Stem Cell Model.Frontiers in genetics · 2021Article
- Article
- Treatment of Epilepsy Associated with Common Chromosomal Developmental Diseases.Open life sciences · 2020Article
- Integrative Analysis Extracts a Core ceRNA Network of the Fetal Hippocampus With Down Syndrome.Frontiers in genetics · 2020Article
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5 authors at 1 institution in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Overinhibition is assumed one of the main causes of cognitive deficits (e.g. memory impairment) in mouse models of Down syndrome (DS). Yet the mechanisms that drive such exaggerated synaptic inhibition and their behavioral effects remain unclear. Here we report the existence of bidirectional alterations to the synaptic inhibition on CA1 pyramidal cells in the Ts2Cje mouse model of DS which are associated to impaired spatial memory. Furthermore, we identify triplication of the kainate receptor (KAR) encoding gene Grik1 as the cause of these phenotypes. Normalization of Grik1 dosage in Ts2Cje mice specifically restored spatial memory and reversed the bidirectional alterations to CA1 inhibition, but not the changes in synaptic plasticity or the other behavioral modifications observed. We propose that modified information gating caused by disturbed inhibitory tone rather than generalized overinhibition underlies some of the characteristic cognitive deficits in DS.
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