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A 型钾通道亚基缺失的小鼠空间学习缺陷。

Spatial learning deficits in mice lacking A-type K(+) channel subunits.

机构信息

Department of Neuroscience, University of Minnesota, Minneapolis, USA.

出版信息

Hippocampus. 2011 Nov;21(11):1152-6. doi: 10.1002/hipo.20877. Epub 2010 Sep 20.

Abstract

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.

摘要

树突中的 Kv4.2 介导的 A 型 K(+) 通道可起到抑制逆行动作电位、限制巧合检测和改变突触特性的作用。由于在海马体中的自然浓度较高,该蛋白的基因缺失会导致 CA1 树突兴奋性增强,以及信号整合时间窗口变宽,这可能对空间学习有影响。在本研究中,我们在 Morris 水迷宫中测试了 Kv4.2 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潜伏期和路径长度延长,以到达隐藏平台,这与减少使用空间搜索策略、转而偏向于重复循环有关。敲除小鼠在基于回忆的探针试验中也没有表现出对目标区域的偏好,但在开始反转学习时,平台位置的改变对它们的影响较小。我们讨论了这种行为差异的可能性,这可能归因于突触可塑性增强,以及承载不同信息的突触通路之间的选择性丧失,这些信息进入 CA1 区域。© 2010 Wiley Periodicals, Inc.

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