Deletion of RAGE Causes Hyperactivity and Increased Sensitivity to Auditory Stimuli in Mice
Deletion of RAGE Causes Hyperactivity and Increased Sensitivity to Auditory Stimuli in Mice
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DOI：
10.1371/journal.pone.0008309
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发表时间：
2009-12-15
期刊：
影响因子：
3.7
通讯作者：
Hirase, Hajime
中科院分区：
文献类型：
--
作者：
Sakatani, Seiichi;Yamada, Kazuyuki;Hirase, Hajime
晚期糖基化终产物受体（receptor for advanced glycation end-products，RECEPTOR）是一种多配体受体，属于细胞表面受体的免疫球蛋白超家族。在糖尿病和阿尔茨海默氏病中，病理进展通过激活阿尔茨海默氏症而加速。然而，到目前为止，在基础条件下，睡眠如何影响总的行为活动模式还没有得到解决。为了寻找在正常小鼠中的功能性作用，对成年的K 0敲除（KO）小鼠进行了一系列标准行为测试。我们观察到在ESTKO中的家笼活动的稳固增加。此外，听觉惊吓反应评估导致KO小鼠对听觉信号的更高敏感性和增加的前脉冲抑制。在Morris水迷宫、经典恐惧条件反射和高架十字迷宫的空间记忆和焦虑行为测试中，KO和野生型之间没有显著差异。我们的研究结果提出了一种可能性，即系统性治疗闭塞的听觉激活可能会对一般活动水平或对听觉刺激的敏感性产生不利影响。
The receptor for advanced glycation end-products (RAGE) is a multi-ligand receptor that belongs to the immunoglobulin superfamily of cell surface receptors. In diabetes and Alzheimer's disease, pathological progression is accelerated by activation of RAGE. However, how RAGE influences gross behavioral activity patterns in basal condition has not been addressed to date. In search for a functional role of RAGE in normal mice, a series of standard behavioral tests were performed on adult RAGE knockout (KO) mice. We observed a solid increase of home cage activity in RAGE KO. In addition, auditory startle response assessment resulted in a higher sensitivity to auditory signal and increased prepulse inhibition in KO mice. There were no significant differences between KO and wild types in behavioral tests for spatial memory and anxiety, as tested by Morris water maze, classical fear conditioning, and elevated plus maze. Our results raise a possibility that systemic therapeutic treatments to occlude RAGE activation may have adverse effects on general activity levels or sensitivity to auditory stimuli.