Normal induction but accelerated decay of LTP in APP+PS1 transgenic mice
Normal induction but accelerated decay of LTP in APP+PS1 transgenic mice
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DOI：
10.1016/j.nbd.2003.11.011
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发表时间：
2004-03-01
影响因子：
6.1
通讯作者：
Tanila, H
中科院分区：
文献类型：
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作者：
Gureviciene, I;Ikonen, S;Tanila, H
携带突变的人APPswe和PSI（A246 E）转基因的小鼠（A/P小鼠）在依赖于记忆的任务中显示出年龄依赖性记忆障碍。此外，小鼠在一天内在水迷宫中表现出正常的学习，但在几天内表现出损伤。我们记录了LTP在切片准备（CA 1）和慢性植入动物（齿状回，或DG）在17-18个月的年龄。基因型在基础突触传递方面没有差异。此外，LTP诱导和其维持超过60分钟没有A/P和对照小鼠之间的差异。然而，fEPSP增强在体内衰减到77%，其最大值在24小时内在A/P小鼠，而在对照组小鼠保持在96%。在A/P小鼠中LTP衰减的时间过程对应于它们的行为障碍，并且表明在齿状回中Abeta积累可能干扰负责记忆巩固的信号转导通路。(C)2004年爱思唯尔公司All rights reserved.
Mice carrying mutated human APPswe and PSI (A246E) transgenes (A/P mice) show age-dependent memory impairment in hippocampus-dependent tasks. Moreover, the mice show normal learning in the water maze within a day but impairment across days. We recorded LTP in a slice preparation (CA1) and in chronically implanted animals (dentate gyrus, or DG) at 17-18 months of age. The genotypes did not differ in the basal synaptic transmission. Also, LTP induction and its maintenance over 60 min did not differ between A/P and control mice. However, the fEPSP enhancement in vivo decayed to 77% of its maximum in 24 h in A/P mice while remaining at 96% in control mice. The time course of the LTP decay in the A/P mice corresponds to their behavioral impairment and indicates that Abeta accumulation in the dentate gyrus may interfere with the signal transduction pathways responsible for memory consolidation. (C) 2004 Elsevier Inc. All rights reserved.