ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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Who cites it
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.
- Meta-Analysis of Down Syndrome Cortical Development Reveals Underdeveloped State of the Science.Frontiers in cellular neuroscience · 2022Pooled it
- Maternal Choline Supplementation in a Mouse Model of Down Syndrome and Alzheimer's Disease Generates Unique Expression Profile Mosaics Within Three Hippocampal Excitatory Neuronal Populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- sAPPα Inhibits Neurite Outgrowth in Primary Mouse Neurons via GABA B Receptor Subunit 1a.eNeuro · 2026Article
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Common pathogenic mechanisms in the hippocampus across neurodegenerative dementias: Alzheimer's disease, Down syndrome, and Parkinson's disease.NPJ dementia · 2026Article
- Dysregulation of astrocyte-secreted pleiotrophin contributes to neuronal structural and functional deficits in Down syndrome.Cell reports · 2025Article
- sAPPα inhibits neurite outgrowth in primary mouse neurons via GABA B Receptor subunit 1a.bioRxiv : the preprint server for biology · 2025Article
- GABAMedComm · 2025Review
- An increased copy number of glycine decarboxylase (GLDC) associated with psychosis reduces extracellular glycine and impairs NMDA receptor function.Molecular psychiatry · 2025Article
- A Dive Into Cerebellar Dysfunction, Motor Deficits and GABAergic Signaling in Down Syndrome.Cureus · 2025Review
- Multisensory gamma stimulation enhances adult neurogenesis and improves cognitive function in male mice with Down Syndrome.PloS one · 2025Article
- Profiling hippocampal neuronal populations reveals unique gene expression mosaics reflective of connectivity-based degeneration in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease.Frontiers in molecular neuroscience · 2025Article
- Exploring perspectives of Dscam for cognitive deficits: a review of multifunction for regulating neural wiring in homeostasis.Frontiers in molecular neuroscience · 2025Review
- Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice.Science signaling · 2024Article
- The role of Down syndrome cell adhesion molecule in Down syndrome.Medical review (2021) · 2024Review
- Maternal choline supplementation protects against age-associated cholinergic and GABAergic basal forebrain neuron degeneration in the Ts65Dn mouse model of Down syndrome and Alzheimer's disease.Neurobiology of disease · 2023Article
- The Drosophila homolog of APP promotes Dscam expression to drive axon terminal growth, revealing interaction between Down syndrome genes.Disease models & mechanisms · 2023Article
- Generation of Urine-Derived Induced Pluripotent Stem Cells and Cerebral Organoids for Modeling Down Syndrome.Stem cell reviews and reports · 2023Article
- DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models.PLoS biology · 2023Article
- Modeling Alzheimer's disease related phenotypes in the Ts65Dn mouse: impact of age on Aβ, Tau, pTau, NfL, and behavior.Frontiers in neuroscience · 2023Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cognitive impairment in Down syndrome (DS) is characterized by deficient learning and memory. Mouse genetic models of DS exhibit impaired cognition in hippocampally mediated behavioral tasks and reduced synaptic plasticity of hippocampal pathways. Enhanced efficiency of GABAergic neurotransmission was implicated in those changes. We have recently shown that signaling through postsynaptic GABA(B) receptors is significantly increased in the dentate gyrus of Ts65Dn mice, a genetic model of DS. Here we examined a role for GABA(B) receptors in cognitive deficits in DS by defining the effect of selective GABA(B) receptor antagonists on behavior and synaptic plasticity of adult Ts65Dn mice. Treatment with the GABA(B) receptor antagonist CGP55845 restored memory of Ts65Dn mice in the novel place recognition, novel object recognition, and contextual fear conditioning tasks, but did not affect locomotion and performance in T-maze. The treatment increased hippocampal levels of brain-derived neurotrophic factor, equally in 2N and Ts65Dn mice. In hippocampal slices, treatment with the GABA(B) receptor antagonists CGP55845 or CGP52432 enhanced long-term potentiation (LTP) in the Ts65Dn DG. The enhancement of LTP was accompanied by an increase in the NMDA receptor-mediated component of the tetanus-evoked responses. These findings are evidence for a contribution of GABA(B) receptors to changes in hippocampal-based cognition in the Ts65Dn mouse. The ability to rescue cognitive performance through treatment with selective GABA(B) receptor antagonists motivates studies to further explore the therapeutic potential of these compounds in people with DS.
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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.