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
{"title":"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","authors":"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","doi":"10.1111/gbb.12852","DOIUrl":null,"url":null,"abstract":"<p>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 (<i>CTNND2</i>) encodes δ-catenin protein, a neuron-specific catenin implicated in many complex neuropsychiatric diseases. Our previous study demonstrated that the deletion of <i>Ctnnd2</i> in mice led to autism-like behaviors. However, to our knowledge, no study has investigated the effects of <i>Ctnnd2</i> deletion on sleep in mice. In this study, we investigated whether the knockout (KO) of exon 2 of the <i>Ctnnd2</i> gene could induce sleep–wake disorders in mice and identified the effects of oral melatonin (MT) supplementation on <i>Ctnnd2</i> KO mice. Our results demonstrated that the <i>Ctnnd2</i> 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 <i>Ctnnd2</i> 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 <i>Ctnnd2</i> gene deletion.</p>","PeriodicalId":50426,"journal":{"name":"Genes Brain and Behavior","volume":"22 4","pages":""},"PeriodicalIF":2.4000,"publicationDate":"2023-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cd/c8/GBB-22-e12852.PMC10393424.pdf","citationCount":"0","resultStr":"{\"title\":\"Melatonin ameliorates sleep–wake disturbances and autism-like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders\",\"authors\":\"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\",\"doi\":\"10.1111/gbb.12852\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>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 (<i>CTNND2</i>) encodes δ-catenin protein, a neuron-specific catenin implicated in many complex neuropsychiatric diseases. Our previous study demonstrated that the deletion of <i>Ctnnd2</i> in mice led to autism-like behaviors. However, to our knowledge, no study has investigated the effects of <i>Ctnnd2</i> deletion on sleep in mice. In this study, we investigated whether the knockout (KO) of exon 2 of the <i>Ctnnd2</i> gene could induce sleep–wake disorders in mice and identified the effects of oral melatonin (MT) supplementation on <i>Ctnnd2</i> KO mice. Our results demonstrated that the <i>Ctnnd2</i> 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 <i>Ctnnd2</i> 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 <i>Ctnnd2</i> gene deletion.</p>\",\"PeriodicalId\":50426,\"journal\":{\"name\":\"Genes Brain and Behavior\",\"volume\":\"22 4\",\"pages\":\"\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2023-06-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cd/c8/GBB-22-e12852.PMC10393424.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Genes Brain and Behavior\",\"FirstCategoryId\":\"102\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/gbb.12852\",\"RegionNum\":4,\"RegionCategory\":\"心理学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BEHAVIORAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genes Brain and Behavior","FirstCategoryId":"102","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/gbb.12852","RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BEHAVIORAL SCIENCES","Score":null,"Total":0}
Melatonin ameliorates sleep–wake disturbances and autism-like behaviors in the Ctnnd2 knock out mouse model of autism spectrum disorders
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.
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.