ArticleExperimental neurology2012
Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 76 citations in OpenAlex.
- Epilepsy Mechanisms in Down Syndrome: Genetic and Pathophysiological Perspectives Across the Lifespan.Journal of clinical medicine · 2026Review
- 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
- Infantile Spasms in Pediatric Down Syndrome: Potential Mechanisms Driving Therapeutic Considerations.Children (Basel, Switzerland) · 2024Review
- Amyloid-β oligomers trigger sex-dependent inhibition of GIRK channel activity in hippocampal neurons in mice.Science signaling · 2024Article
- Domain-selective and sex-dependent regulation of learning and memory in mice by GIRK channel activity in CA1 pyramidal neurons of the dorsal hippocampus.Learning & memory (Cold Spring Harbor, N.Y.) · 2024Article
- Glutamatergic synaptic deficits in the prefrontal cortex of the Ts65Dn mouse model for Down syndrome.Frontiers in neuroscience · 2023Article
- Dyrk1a gene dosage in glutamatergic neurons has key effects in cognitive deficits observed in mouse models of MRD7 and Down syndrome.PLoS genetics · 2021Article
- Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down syndrome.Neuronal signaling · 2021Review
- Physical Exercise Modulates Brain Physiology Through a Network of Long- and Short-Range Cellular Interactions.Frontiers in molecular neuroscience · 2021Review
- Impact of the Olig Family on Neurodevelopmental Disorders.Frontiers in neuroscience · 2021Review
- Rethinking Intellectual Disability from Neuro- to Astro-Pathology.International journal of molecular sciences · 2020Review
- Prefrontal-hippocampal functional connectivity encodes recognition memory and is impaired in intellectual disability.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Down Syndrome Reduces the Sedative Effect of Midazolam in Pediatric Cardiovascular Surgical Patients.Scientific reports · 2020Article
- Unbalanced dendritic inhibition of CA1 neurons drives spatial-memory deficits in the Ts2Cje Down syndrome model.Nature communications · 2019Article
- Enhanced Dendritic Inhibition and Impaired NMDAR Activation in a Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Prenatal treatment with EGCG enriched green tea extract rescues GAD67 related developmental and cognitive defects in Down syndrome mouse models.Scientific reports · 2019Article
- Decreasing the Expression of GABAMolecular neurobiology · 2018Article
- Phosphoproteomic Alterations of Ionotropic Glutamate Receptors in the Hippocampus of the Ts65Dn Mouse Model of Down Syndrome.Frontiers in molecular neuroscience · 2018Article
- Aerobic exercise and a BDNF-mimetic therapy rescue learning and memory in a mouse model of Down syndrome.Scientific reports · 2017Article
- Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome.Neurobiology of disease · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
GABAergic dysfunction is implicated in hippocampal deficits of the Ts65Dn mouse model of Down syndrome (DS). Since Ts65Dn mice overexpress G-protein coupled inward-rectifying potassium (GIRK2) containing channels, we sought to evaluate whether increased GABAergic function disrupts the functioning of hippocampal circuitry. After confirming that GABA(B)/GIRK current density is significantly elevated in Ts65Dn CA1 pyramidal neurons, we compared monosynaptic inhibitory inputs in CA1 pyramidal neurons in response to proximal (stratum radiatum; SR) and distal (stratum lacunosum moleculare; SLM) stimulation of diploid and Ts65Dn acute hippocampal slices. Synaptic GABA(B) and GABA(A) mediated currents evoked by SR stimulation were generally unaffected in Ts65Dn CA1 neurons. However, the GABA(B)/GABA(A) ratios evoked by stimulation within the SLM of Ts65Dn hippocampus were significantly larger in magnitude, consistent with increased GABA(B)/GIRK currents after SLM stimulation. These results indicate that GIRK overexpression in Ts65Dn has functional consequences which affect the balance between GABA(B) and GABA(A) inhibition of CA1 pyramidal neurons, most likely in a pathway specific manner, and may contribute to cognitive deficits reported in these mice.
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