Chronic pentylenetetrazole but not donepezil treatment rescues spatial cognition in Ts65Dn mice, a model for Down syndrome.
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On the promise of pharmacotherapies targeted at cognitive and neurodegenerative components of Down syndromeProspects for Improving Brain Function in Individuals with Down SyndromeNew therapies for treating Down syndrome require quality of life measurementEmerging pharmacotherapies for neurodevelopmental disordersTiming of therapies for Down syndrome: the sooner, the betterMouse models of Down syndrome as a tool to unravel the causes of mental disabilitiesFragile X syndrome and targeted treatment trials.Dendritic spine dysgenesis in autism related disordersPotential for treatment of severe autism in tuberous sclerosis complexCharacterization of PTZ-induced seizure susceptibility in a down syndrome mouse model that overexpresses CSTBGABAA receptor subtypes: Therapeutic potential in Down syndrome, affective disorders, schizophrenia, and autism.Pharmacological approaches to improving cognitive function in Down syndrome: current status and considerations.The use of mouse models to understand and improve cognitive deficits in Down syndrome.Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6b(rd1).Otitis media in a mouse model for Down syndromeLowering beta-amyloid levels rescues learning and memory in a Down syndrome mouse model.Molecular basis of pharmacotherapies for cognition in Down syndromeGene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of Down syndrome.Imbalanced pattern completion vs. separation in cognitive disease: network simulations of synaptic pathologies predict a personalized therapeutics strategy.Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.Adaptive and pathological inhibition of neuroplasticity associated with circadian rhythms and sleepMeeting at the crossroads: common mechanisms in Fragile X and Down syndromeRepeated PTZ treatment at 25-day intervals leads to a highly efficient accumulation of doublecortin in the dorsal hippocampus of rats.Experimental models of Rett syndrome based on Mecp2 dysfunction.Neurofibromin regulation of ERK signaling modulates GABA release and learning.Excitation/inhibition imbalance and impaired synaptic inhibition in hippocampal area CA3 of Mecp2 knockout miceSelective impact of MeCP2 and associated histone deacetylases on the dynamics of evoked excitatory neurotransmissionSpecific targeting of the GABA-A receptor α5 subtype by a selective inverse agonist restores cognitive deficits in Down syndrome mice.Chronic Treatment with a Promnesiant GABA-A α5-Selective Inverse Agonist Increases Immediate Early Genes Expression during Memory Processing in Mice and Rectifies Their Expression Levels in a Down Syndrome Mouse ModelA Sonic hedgehog (Shh) response deficit in trisomic cells may be a common denominator for multiple features of Down syndromeGalantamine improves olfactory learning in the Ts65Dn mouse model of Down syndrome.Identification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling Down syndrome.Environmental enrichment decreases GABAergic inhibition and improves cognitive abilities, synaptic plasticity, and visual functions in a mouse model of Down syndromeIncreased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndromeAdult-onset fluoxetine treatment does not improve behavioral impairments and may have adverse effects on the Ts65Dn mouse model of Down syndrome.Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.Down syndrome and the molecular pathogenesis resulting from trisomy of human chromosome 21.Short-term treatment with the GABAA receptor antagonist pentylenetetrazole produces a sustained pro-cognitive benefit in a mouse model of Down's syndrome.Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Molecular responses of the Ts65Dn and Ts1Cje mouse models of Down syndrome to MK-801.
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P2860
Chronic pentylenetetrazole but not donepezil treatment rescues spatial cognition in Ts65Dn mice, a model for Down syndrome.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh-hant
name
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@en
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@nl
type
label
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@en
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@nl
prefLabel
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@en
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@nl
P2093
P1433
P1476
Chronic pentylenetetrazole but ...... ce, a model for Down syndrome.
@en
P2093
P356
10.1016/J.NEULET.2007.12.039
P407
P577
2008-01-15T00:00:00Z