Spatial learning deficits in mice lacking A-type K(+) channel subunits.
Spatial learning deficits in mice lacking A-type K(+) channel subunits.
复制标题
缺乏 A 型 K( ) 通道亚基的小鼠的空间学习缺陷。
DOI：
10.1002/hipo.20877
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发表时间：
2011
期刊：
影响因子：
3.5
通讯作者：
Yuan,Li-Lian
中科院分区：
文献类型：
--
作者：
Lockridge,Amber;Yuan,Li-Lian
Kv4.2介导的A型K+通道在树突中起抑制反向传播动作电位、限制符合检测和改变突触特性的作用。由于该蛋白在海马区的天然高浓度，该蛋白的基因缺失会导致CA1树突状细胞兴奋性增强，并提供更广泛的信号整合时间窗口，从而可能对空间学习产生影响。在这项研究中，我们在Morris水迷宫中测试了Kv4.2基因敲除小鼠，以评估它们的空间参考获取和回忆能力。这些小鼠在学习试验中表现出到达隐藏平台的潜伏期和路径长度延长，这与减少使用空间搜索策略而有利于重复循环有关。在基于回忆的探测试验中，基因敲除小鼠也没有表现出对目标区域的偏好，但在开始反向学习时，平台位置的改变对小鼠的损害较小。我们讨论了这些行为差异可能归因于突触可塑性的增强和突触通路之间选择性的丧失，这些突触通路携带不同的信息进入CA1区。©2010 Wiley期刊，Inc.
Kv4.2‐mediated A‐type K+channels in dendrites act to dampen back‐propagating action potentials, constrain coincidence detection, and modify synaptic properties. Because of naturally high concentrations in the hippocampus, genetic deletion of this protein results in enhanced CA1 dendritic excitability and a broader signal integration time window with potential implications for spatial learning. In this investigation, we tested Kv4.2 knockout mice in the Morris water maze to assess their spatial reference acquisition and recall abilities. These mice demonstrated prolonged latencies and pathlength to reach a hidden platform during learning trials that was correlated to a decreased use of spatial search strategies in favor of repetitive looping. Knockout mice also showed no preference for target areas in recall‐based probe trials but were less impaired by a switch in the platform location at the start of reversal learning. We discuss the possibility that these behavior discrepancies may be attributable to an enhancement in synaptic plasticity and loss of selectivity among synaptic pathways bearing different information into the CA1 region. © 2010 Wiley Periodicals, Inc.