Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine.
Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine.
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唐氏综合症小鼠模型中 NMDA 介导的 LTD 被夸大，并通过美金刚进行药理救援。
DOI：
10.1101/lm.024182.111
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Costa,AlbertoCS
中科院分区：
文献类型：
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作者：
Scott-McKean,JonahJ;Costa,AlbertoCS
Ts65Dn 小鼠是研究最深入的唐氏综合症动物模型。在此描述的实验中，通过分别在 Ts65Dn 和整倍体对照小鼠的海马切片的 CA1 区域中应用 20 µM NMDA 3 分钟和 50 µM DHPG 5 分钟，诱导 NMDA 介导或 mGluR 介导的 LTD。我们发现，与整倍体对照动物相比，Ts65Dn 小鼠在海马 CA1 区表现出夸大的 NMDA 诱导的 LTD，但不是 mGluR 诱导的。此外，这种异常水平的LTD可以通过NMDA受体拮抗剂美金刚在药理学上得到挽救。
The Ts65Dn mouse is the best-studied animal model for Down syndrome. In the experiments described here, NMDA-mediated or mGluR-mediated LTD was induced in the CA1 region of hippocampal slices from Ts65Dn and euploid control mice by bath application of 20 µM NMDA for 3 min and 50 µM DHPG for 5 min, respectively. We found that Ts65Dn mice display exaggerated NMDA-induced, but not mGluR-induced, LTD in the CA1 region of the hippocampus compared with euploid control animals. In addition, this abnormal level of LTD can be pharmacologically rescued by the NMDA receptor antagonist memantine.