Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome
Top Cited Papers
- 25 February 2007
- journal article
- Published by Springer Nature in Nature Neuroscience
- Vol. 10 (4) , 411-413
- https://doi.org/10.1038/nn1860
Abstract
Ts65Dn mice, a model for Down syndrome, have excessive inhibition in the dentate gyrus, a condition that could compromise synaptic plasticity and mnemonic processing. We show that chronic systemic treatment of these mice with GABAA antagonists at non-epileptic doses causes a persistent post-drug recovery of cognition and long-term potentiation. These results suggest that over-inhibition contributes to intellectual disabilities associated with Down syndrome and that GABAA antagonists may be useful therapeutic agents for this disorder.Keywords
This publication has 14 references indexed in Scilit:
- Mouse Models of Cognitive Disorders in Trisomy 21: A ReviewBehavior Genetics, 2006
- Deficits in hippocampal CA1 LTP induced by TBS but not HFS in the Ts65Dn mouse: A model of Down syndromeNeuroscience Letters, 2005
- Synaptic structural abnormalities in the Ts65Dn mouse model of down syndromeJournal of Comparative Neurology, 2004
- Hippocampal Long-Term Potentiation Suppressed by Increased Inhibition in the Ts65Dn Mouse, a Genetic Model of Down SyndromeJournal of Neuroscience, 2004
- Terpene Trilactones from Ginkgo biloba Are Antagonists of Cortical Glycine and GABAA ReceptorsJournal of Biological Chemistry, 2003
- Down's syndrome: a genetic disorder in biobehavioral perspectiveGenes, Brain and Behavior, 2003
- Synaptic deficit in the temporal cortex of partial trisomy 16 (Ts65Dn) micePublished by Elsevier ,2000
- Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndromeProceedings of the National Academy of Sciences, 1996
- Time-Dependent Processes in Memory StorageScience, 1966
- PHARMACOLOGICAL TREATMENT OF AGED PATIENTS IN A STATE MENTAL HOSPITALPublished by American Medical Association (AMA) ,1953