Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome

被引:189
作者
Siarey, RJ
Stoll, J
Rapoport, SI
Galdzicki, Z [1 ]
机构
[1] NIA, Neurosci Lab, NIH, Bethesda, MD 20892 USA
[2] Texas Tech Univ, Ctr Hlth, Sch Pharm, Amarillo, TX 79106 USA
关键词
Down Syndrome; trisomy; Ts65Dn; long-term potentiation (LTP); hippocampus; mental retardation; learning;
D O I
10.1016/S0028-3908(97)00157-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the phenomenon of long-term potentiation (LTP) in a genetic model of Down Syndrome, the segmental trisomy mouse (Ts65Dn). Ts65Dn mice survive to adulthood and have an extra chromosome that contains a segment of chromosome 16 homologous to human chromosome 21. In this study, field excitatory postsynaptic potentials (fEPSP) were recorded from the CA1 area of in vitro hippocampal slices from diploid and Ts65Dn mice, and LTP was induced by a single tetanizing pulse train (1 sec in duration) at 100 Hz. The hippocampus from both young (2 months) and older (9 months) Ts65Dn mice had a reduced LTP over a period of 60 min compared with LTP in age-matched controls. This finding may explain the reported behavioral and learning impairments in Ts65Dn mice; it suggests that this mouse model can be used to study the role of altered synaptic plasticity in mental retardation of Down Syndrome. Published by Elsevier Science Ltd.
引用
收藏
页码:1549 / 1554
页数:6
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