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Nat Neurosci. 2007 Apr;10(4):411-3. Epub 2007 Feb 25.

Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome.

Author information

1
Department of Psychiatry and Behavioral Sciences, Nancy Pritzker Laboratory, Stanford University, Palo Alto, California 94304-5485, USA.

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.

PMID:
17322876
DOI:
10.1038/nn1860
[Indexed for MEDLINE]

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