The functional nature of synaptic circuitry is altered in area CA3 of the hippocampus in a mouse model of Down's syndrome - Wikidata - thesis-toulmin - TriplyDB

The functional nature of synaptic circuitry is altered in area CA3 of the hippocampus in a mouse model of Down's syndrome

The functional nature of synaptic circuitry is altered in area CA3 of the hippocampus in a mouse model of Down's syndrome

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Mouse models of Down syndrome as a tool to unravel the causes of mental disabilities Hippocampal circuit dysfunction in the Tc1 mouse model of Down syndrome.Synaptopathies: synaptic dysfunction in neurological disorders - A review from students to students Pharmacotherapy with fluoxetine restores functional connectivity from the dentate gyrus to field CA3 in the Ts65Dn mouse model of down syndrome Violence: heightened brain attentional network response is selectively muted in Down syndrome The use of mouse models to understand and improve cognitive deficits in Down syndrome.Lithium rescues synaptic plasticity and memory in Down syndrome mice.Hedgehog agonist therapy corrects structural and cognitive deficits in a Down syndrome mouse model Imbalanced pattern completion vs. separation in cognitive disease: network simulations of synaptic pathologies predict a personalized therapeutics strategy.Developmentally altered inhibition in Ts65Dn, a mouse model of Down syndrome Beyond counts and shapes: studying pathology of dendritic spines in the context of the surrounding neuropil through serial section electron microscopy.A Sonic hedgehog (Shh) response deficit in trisomic cells may be a common denominator for multiple features of Down syndrome The Down syndrome critical region regulates retinogeniculate refinement Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome Trisomy 21 and early brain development Increased excitability and altered action potential waveform in cerebellar granule neurons of the Ts65Dn mouse model of Down syndrome Gene expression changes in the MAPK pathway in both Fragile X and Down syndrome human neural progenitor cells.Involvement of Potassium and Cation Channels in Hippocampal Abnormalities of Embryonic Ts65Dn and Tc1 Trisomic Mice Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome.Altered expression of KIF17, a kinesin motor protein associated with NR2B trafficking, may mediate learning deficits in a Down syndrome mouse model.Heterogeneous reallocation of presynaptic efficacy in recurrent excitatory circuits adapting to inactivity.Abnormal expression of synaptic proteins and neurotrophin-3 in the Down syndrome mouse model Ts65Dn.Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Abnormal brain synchrony in Down Syndrome.Normal protein composition of synapses in Ts65Dn mice: a mouse model of Down syndrome.Down syndrome: from understanding the neurobiology to therapy.A new mouse model for the trisomy of the Abcg1-U2af1 region reveals the complexity of the combinatorial genetic code of down syndrome Aneuploidy: from a physiological mechanism of variance to Down syndrome.Increased Sparsity of Hippocampal CA1 Neuronal Ensembles in a Mouse Model of Down Syndrome Assayed by Arc Expression.The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome Improving Memory and Cognition in Individuals with Down Syndrome.Paired whole cell recordings in organotypic hippocampal slices.Intact long-term potentiation but reduced connectivity between neocortical layer 5 pyramidal neurons in a mouse model of Rett syndrome.Three-dimensional synaptic ultrastructure in the dentate gyrus and hippocampal area CA3 in the Ts65Dn mouse model of Down syndrome.Aerobic exercise and a BDNF-mimetic therapy rescue learning and memory in a mouse model of Down syndrome.Decreasing the Expression of GABAA α5 Subunit-Containing Receptors Partially Improves Cognitive, Electrophysiological, and Morphological Hippocampal Defects in the Ts65Dn Model of Down Syndrome.A third copy of the Down syndrome cell adhesion molecule (Dscam) causes synaptic and locomotor dysfunction in Drosophila.Synaptic mechanisms of pattern completion in the hippocampal CA3 network.Inhibitory modulation of cortical up states.

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The functional nature of synaptic circuitry is altered in area CA3 of the hippocampus in a mouse model of Down's syndrome

http://www.wikidata.org/entity/Q24679420

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2007 nî lūn-bûn

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2007 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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The functional nature of synap ...... mouse model of Down's syndrome

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JPHYSIOL.2006.114868

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The Journal of Physiology

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The functional nature of synap ...... mouse model of Down's syndrome

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Craig C Garner

http://www.w3.org/2001/XMLSchema#string

Daniel V Madison

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Jesse E Hanson

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Martina Blank

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Ricardo A Valenzuela

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P2860

Pair recordings reveal all-silent synaptic connections and the postsynaptic expression of long-term potentiation

A simple method for organotypic cultures of nervous tissue

Simple memory: a theory for archicortex

Down's syndrome.

[Study of somatic chromosomes from 9 mongoloid children.]

Understanding mental retardation in Down's syndrome using trisomy 16 mouse models.

Ensemble dynamics of hippocampal regions CA3 and CA1.

The neuropsychology of Down syndrome: evidence for hippocampal dysfunction.

The recall of events through the learning of associations between their parts.

Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: a model of Down syndrome.

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53-67

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Pt 1

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579

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2007-02-15T00:00:00Z

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17158177

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