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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 579/1/53    most recent jphysiol.2006.114868v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hanson, J. E. Articles by Madison, D. V. Search for Related Content PubMed PubMed Citation Articles by Hanson, J. E. Articles by Madison, D. V. Related Collections Neuroscience

¹ Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305-5345, USA
² Department of Psychiatry and Behavioral Science, Nancy Pritzker Laboratory, Stanford University, Palo Alto, CA 94304-5485, USA

Down's syndrome (DS) is the most common cause of mental retardation, and memory impairments are more severe in DS than in most if not all other causes of mental retardation. The Ts65Dn mouse, a genetic model of DS, exhibits phenotypes of DS, including memory impairments indicative of hippocampal dysfunction. We examined functional synaptic connectivity in area CA3 of the hippocampus of Ts65Dn mice using organotypic slice cultures as a model. We found reductions in multiple measures of synaptic function in both excitatory and inhibitory inputs to pyramidal neurons in CA3 of the Ts65Dn hippocampus. However, associational synaptic connections between pyramidal neurons were more abundant and more likely to be active rather than silent in the Ts65Dn hippocampus. Synaptic potentiation was normal in these associational connections. Decreased overall functional synaptic input onto pyramidal neurons expressed along with the specific hyperconnectivity of associational connections between pyramidal neurons will result in predictable alterations of CA3 network function, which may contribute to the memory impairments seen in DS.

(Received 6 June 2006; accepted after revision 29 November 2006; first published online 7 December 2006)
Corresponding author D. V. Madison: Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305-5345, USA. Email: madison{at}stanford.edu

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