白细胞介素1受体辅助蛋白样1基因敲除小鼠表现出脊柱密度降低、学习缺陷、多动以及焦虑样行为减少。
IL1RAPL1 knockout mice show spine density decrease, learning deficiency, hyperactivity and reduced anxiety-like behaviours.
作者信息
Yasumura Misato, Yoshida Tomoyuki, Yamazaki Maya, Abe Manabu, Natsume Rie, Kanno Kouta, Uemura Takeshi, Takao Keizo, Sakimura Kenji, Kikusui Takefumi, Miyakawa Tsuyoshi, Mishina Masayoshi
机构信息
1] Department of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan [2] Liaison Academy, School of Medicine, University of Yamanashi, Chuo, Yamanashi, Japan.
1] Department of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan [2] Department of Molecular Neuroscience, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Toyama, Japan [3] PRESTO, Japan Science and Technology Agency, Kawaguchi, Saitama, Japan.
出版信息
Sci Rep. 2014 Oct 14;4:6613. doi: 10.1038/srep06613.
IL-1 receptor accessory protein-like 1 (IL1RAPL1) is responsible for nonsyndromic intellectual disability and is associated with autism. IL1RAPL1 mediates excitatory synapse formation through trans-synaptic interaction with PTPδ. Here, we showed that the spine density of cortical neurons was significantly reduced in IL1RAPL1 knockout mice. The spatial reference and working memories and remote fear memory were mildly impaired in IL1RAPL1 knockout mice. Furthermore, the behavioural flexibility was slightly reduced in the T-maze test. Interestingly, the performance of IL1RAPL1 knockout mice in the rotarod test was significantly better than that of wild-type mice. Moreover, IL1RAPL1 knockout mice consistently exhibited high locomotor activity in all the tasks examined. In addition, open-space and height anxiety-like behaviours were decreased in IL1RAPL1 knockout mice. These results suggest that IL1RAPL1 ablation resulted in spine density decrease and affected not only learning but also behavioural flexibility, locomotor activity and anxiety.
白细胞介素-1受体辅助蛋白样1（IL1RAPL1）与非综合征性智力障碍相关，并与自闭症有关。IL1RAPL1通过与PTPδ的反式突触相互作用介导兴奋性突触的形成。在此，我们发现IL1RAPL1基因敲除小鼠皮质神经元的棘突密度显著降低。IL1RAPL1基因敲除小鼠的空间参考记忆、工作记忆和远期恐惧记忆轻度受损。此外，在T迷宫试验中，其行为灵活性略有降低。有趣的是，IL1RAPL1基因敲除小鼠在转棒试验中的表现明显优于野生型小鼠。而且，在所有检测任务中，IL1RAPL1基因敲除小鼠始终表现出较高的运动活性。此外，IL1RAPL1基因敲除小鼠的旷场和高架零迷宫焦虑样行为减少。这些结果表明，IL1RAPL1基因缺失导致棘突密度降低，不仅影响学习，还影响行为灵活性、运动活性和焦虑。
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