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在过表达小电导钙激活钾离子通道2型(KCa2.2,SK2)的小鼠中观察到的情境记忆缺陷是由编码缺陷引起的。

Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit.

作者信息

Stackman Robert W, Bond Chris T, Adelman John P

机构信息

Program in Psychobiology, Department of Psychology, Florida Atlantic University, Boca Raton, Florida 33431-0991, USA.

出版信息

Learn Mem. 2008 Mar 27;15(4):208-13. doi: 10.1101/lm.906808. Print 2008 Apr.

Abstract

Hippocampal-dependent synaptic plasticity and memory are modulated by apamin-sensitive small conductance Ca2+-activated K+ (SK) channels. Transgenic mice overexpressing SK2 channels (SK2+/T mice) exhibit marked deficits in hippocampal memory and synaptic plasticity, as previously reported. Here, we examined whether SK2 overexpression affects the encoding or retention of contextual memory. Compared with wild-type littermates, SK2+/T mice exhibited significantly less context-dependent freezing 10 min and 24 h after conditioning. Interestingly, this contextual memory impairment was eliminated if SK2+/T mice were permitted longer pre-exposure to the conditioning chamber. These data support converging evidence that SK2 channels restrict the encoding of hippocampal memory.

摘要

海马体依赖的突触可塑性和记忆受蜂毒明肽敏感的小电导钙激活钾(SK)通道调节。如先前报道,过表达SK2通道的转基因小鼠(SK2+/T小鼠)在海马体记忆和突触可塑性方面表现出明显缺陷。在此,我们研究了SK2过表达是否会影响情境记忆的编码或保持。与野生型同窝小鼠相比,SK2+/T小鼠在条件反射后10分钟和24小时表现出显著更少的情境依赖性僵立。有趣的是,如果允许SK2+/T小鼠更长时间预先暴露于条件反射箱,这种情境记忆损伤会被消除。这些数据支持了越来越多的证据,即SK2通道限制海马体记忆的编码。

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