Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit
Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit
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DOI：
10.1101/lm.906808
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发表时间：
2008-04-01
影响因子：
2
通讯作者：
Adelman, John P.
中科院分区：
文献类型：
--
作者：
Stackman, Robert W., Jr.;Bond, Chris T.;Adelman, John P.
海马依赖的突触可塑性和记忆是由apamin敏感的小电导钙激活的K+（SK）通道调制。如前所述，过度表达SK2通道的转基因小鼠（SK2+/ T小鼠）表现出海马记忆和突触可塑性的明显缺陷。在这里，我们研究了SK2过表达是否影响上下文记忆的编码或保留。与野生型同窝小鼠相比，SK2+/ T小鼠在条件化后10 min和24 h表现出显著更少的情境依赖性冻结。有趣的是，如果允许SK2+/ T小鼠更长时间地预暴露于条件化室，则这种背景记忆障碍被消除。这些数据支持了SK2通道限制海马记忆编码的证据。
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.