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Article

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

22 Mar 2017

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 28342823
DOI: 10.1016/j.nbd.2017.03.009

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Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndromePMID 28342823Read ↗

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Overexpression of Dyrk1A Is Implicated in Several Cognitive, Electrophysiological and Neuromorphological Alterations Found in a Mouse Model of Down SyndromeSemantic proximity Read ↗

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Abnormal expression of synaptic proteins and neurotrophin-3 in the down syndrome mouse model Ts65DnSemantic proximity Read ↗

Hippocampal volume and neuronal number in Ts65Dn mice: a murine model of down syndromeSemantic proximity Read ↗

Altered long-term potentiation in the young and old Ts65Dn mouse, a model for down syndromeSemantic proximity Read ↗

Abnormal synaptic plasticity in the Ts1Cje segmental trisomy 16 mouse model of Down syndromeSemantic proximity Read ↗

Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships.Semantic proximity Read ↗

Mouse models of Down syndrome: gene content and consequencesSemantic proximity Read ↗

The "Down syndrome critical region" is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome.Semantic proximity Read ↗

Alteration of inhibitory circuits in the somatosensory cortex of Ts65Dn mice, a model for Down’s syndromeSemantic proximity Read ↗

Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6b(rd1).Semantic proximity Read ↗

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