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DYRK1A BAC transgenic mice show altered synaptic plasticity with learning and memory defects

Authors :
Kyoung-Jin Ahn
Hey Kyeong Jeong
Han-Saem Choi
Soo-Ryoon Ryoo
Yeon Ju Kim
Jun-Seo Goo
Se-Young Choi
Jung-Soo Han
Ilho Ha
Woo-Joo Song
Source :
Neurobiology of Disease, Vol 22, Iss 3, Pp 463-472 (2006)
Publication Year :
2006
Publisher :
Elsevier, 2006.

Abstract

Among the various phenotypes seen in Down syndrome (DS), mental retardation is the most common and most debilitating condition suffered by individuals with DS. The DYRK1A gene on human chromosome 21q22.2 encodes a subfamily of protein kinases that displays dual substrate specificities and is known to play a critical role in neurodevelopment. To study DS mental retardation, we have generated transgenic mice that contain only one copy of the complete human DYRK1A gene in a bacterial artificial chromosome. The transgenic mice showed significant impairment in hippocampal-dependent memory tasks in a Morris water maze. Interestingly, we observed shifts in both long-term potentiation and long-term depression, which suggests a role for DYRK1A in bidirectional synaptic plasticity. These mice represent the most clinically relevant DYRK1A mouse model to date and provide us a valuable tool for the in vivo study of mechanisms that underlie the learning and memory deficit in DS.

Details

Language :
English
ISSN :
1095953X
Volume :
22
Issue :
3
Database :
Directory of Open Access Journals
Journal :
Neurobiology of Disease
Publication Type :
Academic Journal
Accession number :
edsdoj.35443fbc1e4527981a3b8a0bda5c65
Document Type :
article
Full Text :
https://doi.org/10.1016/j.nbd.2005.12.006