Gang Chen , Xingyao Chen , Wei Han , Baoyao Gao , Min Liang , Tao Li , Xinshe Liu
{"title":"MiR-222-3p通过PP2A-AKT信号通路调节雄性小鼠背侧纹状体中甲基苯丙胺诱导的行为致敏。","authors":"Gang Chen , Xingyao Chen , Wei Han , Baoyao Gao , Min Liang , Tao Li , Xinshe Liu","doi":"10.1016/j.neulet.2025.138181","DOIUrl":null,"url":null,"abstract":"<div><div>Drug addiction is a chronic and recurrent brain disease. Our previous research demonstrated that the B subunit of phosphatase 2A (PP2A/B) increased in the dorsal striatum (DS) of methamphetamine (METH)-sensitized mice. Interestingly, studies indicate that PP2A/B can also interplay with microRNA (miRNA). In this study, we investigated seven miRNAs that have been reported to potentially interplay with PP2A/B, and our results showed that miR-222-3p significantly decreased in the DS of METH-sensitized mice. We further used dual-luciferase reporter assay to clarify the regulatory relationship between miR-222-3p and PP2A/B mRNA, and we also constructed adeno-associated virus (AAV) to overexpress miR-222-3p in the DS to further examine the influence of miR-222-3p on METH-induced behavioral sensitization. Our results demonstrated that miR-222-3p did interplay with PP2A/B mRNA and overexpressed miR-222-3p could significant attenuate METH-induced behavioral sensitization. At the same time, overexpressed miR-222-3p could reverse the change in the PP2A–AKT signaling pathway in the DS of METH-sensitized mice. Our results indicate that overexpression of miR-222-3p in the DS might attenuate METH-induced behavioral sensitization through the PP2A–AKT signaling pathway.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"852 ","pages":"Article 138181"},"PeriodicalIF":2.5000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MiR-222-3p regulates methamphetamine-induced behavioral sensitization through PP2A–AKT signaling pathway in the dorsal striatum of male mice\",\"authors\":\"Gang Chen , Xingyao Chen , Wei Han , Baoyao Gao , Min Liang , Tao Li , Xinshe Liu\",\"doi\":\"10.1016/j.neulet.2025.138181\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Drug addiction is a chronic and recurrent brain disease. Our previous research demonstrated that the B subunit of phosphatase 2A (PP2A/B) increased in the dorsal striatum (DS) of methamphetamine (METH)-sensitized mice. Interestingly, studies indicate that PP2A/B can also interplay with microRNA (miRNA). In this study, we investigated seven miRNAs that have been reported to potentially interplay with PP2A/B, and our results showed that miR-222-3p significantly decreased in the DS of METH-sensitized mice. We further used dual-luciferase reporter assay to clarify the regulatory relationship between miR-222-3p and PP2A/B mRNA, and we also constructed adeno-associated virus (AAV) to overexpress miR-222-3p in the DS to further examine the influence of miR-222-3p on METH-induced behavioral sensitization. Our results demonstrated that miR-222-3p did interplay with PP2A/B mRNA and overexpressed miR-222-3p could significant attenuate METH-induced behavioral sensitization. At the same time, overexpressed miR-222-3p could reverse the change in the PP2A–AKT signaling pathway in the DS of METH-sensitized mice. Our results indicate that overexpression of miR-222-3p in the DS might attenuate METH-induced behavioral sensitization through the PP2A–AKT signaling pathway.</div></div>\",\"PeriodicalId\":19290,\"journal\":{\"name\":\"Neuroscience Letters\",\"volume\":\"852 \",\"pages\":\"Article 138181\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroscience Letters\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0304394025000692\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Letters","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304394025000692","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
MiR-222-3p regulates methamphetamine-induced behavioral sensitization through PP2A–AKT signaling pathway in the dorsal striatum of male mice
Drug addiction is a chronic and recurrent brain disease. Our previous research demonstrated that the B subunit of phosphatase 2A (PP2A/B) increased in the dorsal striatum (DS) of methamphetamine (METH)-sensitized mice. Interestingly, studies indicate that PP2A/B can also interplay with microRNA (miRNA). In this study, we investigated seven miRNAs that have been reported to potentially interplay with PP2A/B, and our results showed that miR-222-3p significantly decreased in the DS of METH-sensitized mice. We further used dual-luciferase reporter assay to clarify the regulatory relationship between miR-222-3p and PP2A/B mRNA, and we also constructed adeno-associated virus (AAV) to overexpress miR-222-3p in the DS to further examine the influence of miR-222-3p on METH-induced behavioral sensitization. Our results demonstrated that miR-222-3p did interplay with PP2A/B mRNA and overexpressed miR-222-3p could significant attenuate METH-induced behavioral sensitization. At the same time, overexpressed miR-222-3p could reverse the change in the PP2A–AKT signaling pathway in the DS of METH-sensitized mice. Our results indicate that overexpression of miR-222-3p in the DS might attenuate METH-induced behavioral sensitization through the PP2A–AKT signaling pathway.
期刊介绍:
Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.