4.4 Article

Deletion of neuronal gap junction protein connexin 36 impairs hippocampal LTP

期刊

NEUROSCIENCE LETTERS
卷 502, 期 1, 页码 30-32

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.07.018

关键词

Gap junctions; Connexin 36; LTP; Hippocampus; NMDA receptors

资金

  1. NIH [R01 NS064256]
  2. University of Kansas Medical Center

向作者/读者索取更多资源

In the mammalian CNS, deletion of neuronal gap junction protein, connexin 36 (Cx36), causes deficiencies in learning and memory. Here we tested whether Cx36 deletion affects the hippocampal long-term potentiation (LTP), which is considered as a cellular model of learning and memory mechanisms. We report that in acute slices of the hippocampal CA1 area, LTP is reduced in Cx36 knockout mice as compared to wild-type mice. Western blot analysis of NMDA receptor subunits indicates a higher NR2A/NR2B ratio in Cx36 knockout mice, indicating that there is shift in the threshold for LTP induction in knockout animals. Data suggest a possibility that learning and memory deficiencies in Cx36 knockout mice are due to deficiencies in LTP mechanisms. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.4
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据