Melatonin ameliorates sleep–wake disturbances and autism-like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders

IF 2.4 4区 心理学 Q2 BEHAVIORAL SCIENCES
Man Xu, Luyi Wang, Yan Wang, Jing Deng, Xiaoya Wang, Feifei Wang, Sen Pan, Yu Zhao, Ailing Liao, Xiaoqing Wang, Di Chen, Jingjing Shen, Feng Yang, Yingbo Li, Shali Wang
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Abstract

Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder characterized by atypical patterns of social interaction and communication, as well as restrictive and repetitive behaviors. In addition, patients with ASD often presents with sleep disturbances. Delta (δ) catenin protein 2 (CTNND2) encodes δ-catenin protein, a neuron-specific catenin implicated in many complex neuropsychiatric diseases. Our previous study demonstrated that the deletion of Ctnnd2 in mice led to autism-like behaviors. However, to our knowledge, no study has investigated the effects of Ctnnd2 deletion on sleep in mice. In this study, we investigated whether the knockout (KO) of exon 2 of the Ctnnd2 gene could induce sleep–wake disorders in mice and identified the effects of oral melatonin (MT) supplementation on Ctnnd2 KO mice. Our results demonstrated that the Ctnnd2 KO mice exhibited ASD-like behaviors and sleep–wake disorders that were partially attenuated by MT supplementation. Overall, our current study is the first to identify that knockdown of Ctnnd2 gene could induce sleep–wake disorders in mice and suggests that treatment of sleep–wake disturbances by MT may benefit to autism-like behaviors causing by Ctnnd2 gene deletion.

Abstract Image

在ctnd2基因敲除的自闭症谱系障碍小鼠模型中,褪黑素改善了睡眠-觉醒障碍和自闭症样行为
自闭症谱系障碍(ASD)是一种普遍的神经发育障碍,其特征是社会互动和沟通的非典型模式,以及限制性和重复性行为。此外,ASD患者通常表现为睡眠障碍。δ (δ)连环蛋白2 (CTNND2)编码δ-连环蛋白,δ-连环蛋白是一种神经元特异性的连环蛋白,与许多复杂的神经精神疾病有关。我们之前的研究表明,Ctnnd2在小鼠中的缺失会导致自闭症样行为。然而,据我们所知,还没有研究调查过Ctnnd2缺失对小鼠睡眠的影响。在这项研究中,我们研究了Ctnnd2基因外显子2的敲除(KO)是否会诱导小鼠睡眠-觉醒障碍,并确定了口服褪黑激素(MT)补充对Ctnnd2 KO小鼠的影响。我们的研究结果表明,Ctnnd2 KO小鼠表现出asd样行为和睡眠-觉醒障碍,这些行为和障碍通过补充MT部分减轻。总的来说,我们目前的研究首次发现Ctnnd2基因敲低可诱导小鼠睡眠-觉醒障碍,并提示MT治疗睡眠-觉醒障碍可能有利于Ctnnd2基因缺失引起的自闭症样行为。
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来源期刊
Genes Brain and Behavior
Genes Brain and Behavior 医学-行为科学
CiteScore
6.80
自引率
4.00%
发文量
62
审稿时长
4-8 weeks
期刊介绍: Genes, Brain and Behavior was launched in 2002 with the aim of publishing top quality research in behavioral and neural genetics in their broadest sense. The emphasis is on the analysis of the behavioral and neural phenotypes under consideration, the unifying theme being the genetic approach as a tool to increase our understanding of these phenotypes. Genes Brain and Behavior is pleased to offer the following features: 8 issues per year online submissions with first editorial decisions within 3-4 weeks and fast publication at Wiley-Blackwells High visibility through its coverage by PubMed/Medline, Current Contents and other major abstracting and indexing services Inclusion in the Wiley-Blackwell consortial license, extending readership to thousands of international libraries and institutions A large and varied editorial board comprising of international specialists.
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