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

机译:Kv4.2电压门控钾离子通道基因缺失对小鼠焦虑,恐惧和应激相关行为的影响

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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.
机译:背景技术已经提出钾通道在神经可塑性机制中起作用,并且Kv4.2亚基已参与调节向树突的动作电位反向传播。进一步提出了可塑性机制的改变是各种精神疾病的基础,但是人们对Kv4.2在焦虑或抑郁中的作用还没有很好的了解。方法在本文中,我们根据表现型Kv4.2基因敲除的小鼠的神经功能,一系列与焦虑和抑郁相关的行为以及与可塑性相关的学习任务,对它们进行了分析。结果我们在基因敲除小鼠中发现了新奇诱导的过度活跃表型,并且这些小鼠还表现出了对新刺激(如听觉调)的反应性。没有观察到明显的焦虑或抑郁相关表型,也没有基于学习/可塑性的范例的任何改变。结论我们没有找到明确的证据表明Kv4.2参与神经精神病学或可塑性相关的表型,但有人支持Kv4.2在抑制对新刺激的兴奋性反应中的作用。

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