Specific targeting of the GABA-A receptor α5 subtype by a selective inverse agonist restores cognitive deficits in Down syndrome mice.
about
Pathophysiological power of improper tonic GABA(A) conductances in mature and immature models.Prospects for Improving Brain Function in Individuals with Down SyndromeBuilding an adaptive brain across development: targets for neurorehabilitation must begin in infancyMouse models of Down syndrome as a tool to unravel the causes of mental disabilitiesFunctional regulation of GABAA receptors in nervous system pathologiesNeurological phenotypes for Down syndrome across the life spanDown Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 HomologuesMonoacylglycerol lipase inhibitor JZL184 improves behavior and neural properties in Ts65Dn mice, a model of down syndromeSelective Pharmacological Augmentation of Hippocampal Activity Produces a Sustained Antidepressant-Like Response without Abuse-Related or Psychotomimetic EffectsGABA receptor subunit distribution and FMRP-mGluR5 signaling abnormalities in the cerebellum of subjects with schizophrenia, mood disorders, and autism.GABAA 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.Hedgehog agonist therapy corrects structural and cognitive deficits in a Down syndrome mouse modelModulation 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 sleepDifferential Alteration in Expression of Striatal GABAAR Subunits in Mouse Models of Huntington's DiseaseOverexpression of Dyrk1A is implicated in several cognitive, electrophysiological and neuromorphological alterations found in a mouse model of Down syndromeTonic inhibition in dentate gyrus impairs long-term potentiation and memory in an Alzheimer's [corrected] disease model.The App-Runx1 region is critical for birth defects and electrocardiographic dysfunctions observed in a Down syndrome mouse model.Protein dynamics associated with failed and rescued learning in the Ts65Dn mouse model of Down syndrome.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 syndromeIdentification of the translocation breakpoints in the Ts65Dn and Ts1Cje mouse lines: relevance for modeling Down syndrome.Trisomy 21 and early brain developmentTc1 mouse model of trisomy-21 dissociates properties of short- and long-term recognition memory.Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeuticsFrom abnormal hippocampal synaptic plasticity in down syndrome mouse models to cognitive disability in down syndrome.Adult-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.Pharmacological correction of excitation/inhibition imbalance in Down syndrome mouse models.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.Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficitsDisinhibition, an emerging pharmacology of learning and memoryThe GABAergic Hypothesis for Cognitive Disabilities in Down SyndromeBenzodiazepine receptor ligands: a patent review (2006-2012).GABAergic dysfunction in pediatric neuro-developmental disorders.Neural oscillations during non-rapid eye movement sleep as biomarkers of circuit dysfunction in schizophrenia.Altered Intrinsic Pyramidal Neuron Properties and Pathway-Specific Synaptic Dysfunction Underlie Aberrant Hippocampal Network Function in a Mouse Model of Tauopathy.Dentate gyrus mediates cognitive function in the Ts65Dn/DnJ mouse model of Down syndrome.
P2860
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P2860
Specific targeting of the GABA-A receptor α5 subtype by a selective inverse agonist restores cognitive deficits in Down syndrome mice.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@ast
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@en
type
label
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@ast
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@en
prefLabel
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@ast
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@en
P2093
P2860
P356
P1476
Specific targeting of the GABA ...... eficits in Down syndrome mice.
@en
P2093
B Delatour
F de Chaumont
J-C Olivo-Marin
L Dauphinot
M-C Potier
P Lopes Pereira
P2860
P304
P356
10.1177/0269881111405366
P407
P577
2011-06-21T00:00:00Z