Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome
Altered long-term potentiation in the young and old Ts65Dn mouse, a model for Down Syndrome
复制标题
DOI：
10.1016/s0028-3908(97)00157-3
复制
发表时间：
1997-11-01
影响因子：
4.7
通讯作者：
Galdzicki, Z
中科院分区：
文献类型：
--
作者：
Siarey, RJ;Stoll, J;Galdzicki, Z
我们研究了唐氏综合征的遗传模型-节段性三体小鼠(Ts65Dn)的长时程增强(LTP)现象。Ts65Dn小鼠存活到成年，并拥有一条额外的染色体，其中包含一段与人类21号染色体同源的16号染色体。在本研究中，记录了二倍体和Ts65Dn小鼠体外海马脑片CA1区场兴奋性突触后电位(FEPSP)，并用100赫兹的单个破伤风脉冲序列(持续1秒)诱发LTP。与年龄匹配的对照组相比，年轻(2个月)和老年(9个月)Ts65Dn小鼠的海马体在60分钟内LTP降低。这一发现可能解释了已报道的Ts65Dn小鼠的行为和学习障碍；这表明该小鼠模型可用于研究突触可塑性改变在唐氏综合征智力低下中的作用。爱思唯尔科学有限公司出版。
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.