Effects of genetic deletion of the Kv4.2 voltage-gated potassium channel on murine anxiety-, fear- and stress-related behaviors.

Carly Kiselycznyk, Dax A Hoffman, Andrew Holmes
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引用次数: 8

Abstract

Background: Potassium channels have been proposed to play a role in mechanisms of neural plasticity, and the Kv4.2 subunit has been implicated in the regulation of action-potential back-propagation to the dendrites. Alterations in mechanisms of plasticity have been further proposed to underlie various psychiatric disorders, but the role of Kv4.2 in anxiety or depression is not well understood.

Methods: In this paper, we analyzed the phenotype Kv4.2 knockout mice based on their neurological function, on a battery of behaviors including those related to anxiety and depression, and on plasticity-related learning tasks.

Results: We found a novelty-induced hyperactive phenotype in knockout mice, and these mice also displayed increased reactivity to novel stimulus such as an auditory tone. No clear anxiety- or depression-related phenotype was observed, nor any alterations in learning/plasticity-based paradigms.

Conclusions: We did not find clear evidence for an involvement of Kv4.2 in neuropsychiatric or plasticity-related phenotypes, but there was support for a role in Kv4.2 in dampening excitatory responses to novel stimuli.

Abstract Image

Abstract Image

Abstract Image

Kv4.2电压门控钾通道基因缺失对小鼠焦虑、恐惧和应激相关行为的影响
背景:钾通道被认为在神经可塑性机制中发挥作用,Kv4.2亚基参与了动作电位向树突反向传播的调节。可塑性机制的改变已被进一步提出作为各种精神疾病的基础,但Kv4.2在焦虑或抑郁中的作用尚未得到很好的理解。方法:在本文中,我们根据Kv4.2基因敲除小鼠的神经功能、与焦虑和抑郁相关的一系列行为以及与可塑性相关的学习任务来分析表型。结果:我们在敲除小鼠中发现了一种新颖性诱导的过度活跃表型,这些小鼠对新颖性刺激(如听觉音调)的反应性也有所增加。没有观察到明显的焦虑或抑郁相关表型,也没有任何基于学习/可塑性的范式的改变。结论:我们没有发现明确的证据表明Kv4.2参与神经精神或可塑性相关表型,但有证据支持Kv4.2在抑制对新刺激的兴奋反应中起作用。
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