Corrigendum to "TRPC3 channels critically regulate hippocampal excitability and contextual fear memory" Behav. Brain Res. 281(March) 2015, 69-77.
Corrigendum to "TRPC3 channels critically regulate hippocampal excitability and contextual fear memory" Behav. Brain Res. 281(March) 2015, 69-77.
复制标题
“TRPC3 通道严格调节海马兴奋性和情境恐惧记忆”行为的勘误。
DOI：
10.1016/j.bbr.2017.05.038
复制
发表时间：
2017
影响因子：
2.7
通讯作者：
Kaczorowski,CatherineC
中科院分区：
文献类型：
--
作者：
Neuner,SarahM;Wilmott,LyndaA;Hope,KevinA;Hoffmann,Brian;Chong,JayhongA;Abramowitz,Joel;Birnbaumer,Lutz;O'Connell,Kristen;Tryba,AndrewK;Greene,AndrewS;Chan,CSavio;Kaczorowski,CatherineC
报告了Sarah M.作者：Lynda A.作者：Kevin A.放大图片作者：Brian Hoffmann，Jayhong A.放大图片作者：Joel Abramowitz，Lutz Birnbaumer，Kristen M.作者声明：Andrew K.作者：Andrew S.格林角Savio Chan和Catherine C. Kaczorowski（Behavioural Brain Research，2015 [Mar][15]，281，69-77）。在原文中，在结果部分的第4段中有一些数字错误。此外，在手稿的方法部分，mTrpC 3 shRNA序列中省略了一个核苷酸。勘误表中给出了更正，图3的标题已被修改以反映这些变化。(The原始文章的以下摘要出现在记录2015-04681-010中）。记忆的形成需要从头蛋白质合成，记忆障碍可能是由于关键蛋白质的合成失调而导致的，这些蛋白质在很大程度上仍未被识别。考虑到质膜离子通道和受体在调节神经元兴奋性（一种候选记忆机制）中的作用，它们可能是候选者。在这里，我们进行有针对性的分子监测和定量海马质膜蛋白与完整或受损的上下文恐惧记忆的小鼠，以确定推定的候选人。在这里，我们报告上下文恐惧记忆缺陷对应于增加的Trpc 3基因和蛋白质表达，并证明TRPC 3调节海马神经元兴奋性与记忆功能。这些数据提供了在海马中TRPC 3敲低后本文报道的增强的背景恐惧记忆的机制解释。总的来说，TRPC 3调节记忆，可能是增强记忆和治疗记忆障碍的可行靶点。（PsycInfo数据库记录（c）2020阿帕，保留所有权利）
Reports an error in" TRPC3 channels critically regulate hippocampal excitability and contextual fear memory" by Sarah M. Neuner, Lynda A. Wilmott, Kevin A. Hope, Brian Hoffmann, Jayhong A. Chong, Joel Abramowitz, Lutz Birnbaumer, Kristen M. O'Connell, Andrew K. Tryba, Andrew S. Greene, C. Savio Chan and Catherine C. Kaczorowski (Behavioural Brain Research, 2015 [Mar][15], Vol 281, 69-77). In the original article, there were some numerical errors in the 4 th paragraph of the results section. In addition, a nucleotide was omitted from the sequence of mTrpC3 shRNA in the methods section of the manuscript. The corrections are present in the erratum, and Fig. 3 captions ahve been revised to reflect these changes.(The following abstract of the original article appeared in record 2015-04681-010). Memory formation requires de novo protein synthesis, and memory disorders may result from misregulated synthesis of critical proteins that remain largely unidentified. Plasma membrane ion channels and receptors are likely candidates given their role in regulating neuron excitability, a candidate memory mechanism. Here we conduct targeted molecular monitoring and quantitation of hippocampal plasma membrane proteins from mice with intact or impaired contextual fear memory to identify putative candidates. Here we report contextual fear memory deficits correspond to increased Trpc3 gene and protein expression, and demonstrate TRPC3 regulates hippocampal neuron excitability associated with memory function. These data provide a mechanistic explanation for enhanced contextual fear memory reported herein following knockdown of TRPC3 in hippocampus. Collectively, TRPC3 modulates memory and may be a feasible target to enhance memory and treat memory disorders.(PsycInfo Database Record (c) 2020 APA, all rights reserved)