{"title":"n型Ca2+通道介导小鼠纹状体刺激依赖性α-突触核蛋白分泌。","authors":"Emmanouela Leandrou,Ioanna Chalatsa,Kostas Vekrellis,Evangelia Emmanouilidou","doi":"10.1038/s41531-025-01110-z","DOIUrl":null,"url":null,"abstract":"The secretion of α-synuclein from presynaptic terminals is controlled by neuronal activity through a calcium-dependent mechanism. To address the role of voltage gated calcium channels in this process, we used reverse brain microdialysis to monitor α-synuclein release in vivo in the presence of selective channel inhibitors. Our results revealed that the ω-conotoxin GVIA-sensitive N-type calcium channels are the major mediators of stimulated α-synuclein secretion in mouse striatum.","PeriodicalId":19706,"journal":{"name":"NPJ Parkinson's Disease","volume":"93 1","pages":"276"},"PeriodicalIF":8.2000,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"N-type Ca2+ channels mediate the stimuli-dependent α-synuclein secretion in mouse striatum.\",\"authors\":\"Emmanouela Leandrou,Ioanna Chalatsa,Kostas Vekrellis,Evangelia Emmanouilidou\",\"doi\":\"10.1038/s41531-025-01110-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The secretion of α-synuclein from presynaptic terminals is controlled by neuronal activity through a calcium-dependent mechanism. To address the role of voltage gated calcium channels in this process, we used reverse brain microdialysis to monitor α-synuclein release in vivo in the presence of selective channel inhibitors. Our results revealed that the ω-conotoxin GVIA-sensitive N-type calcium channels are the major mediators of stimulated α-synuclein secretion in mouse striatum.\",\"PeriodicalId\":19706,\"journal\":{\"name\":\"NPJ Parkinson's Disease\",\"volume\":\"93 1\",\"pages\":\"276\"},\"PeriodicalIF\":8.2000,\"publicationDate\":\"2025-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"NPJ Parkinson's Disease\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41531-025-01110-z\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"NPJ Parkinson's Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41531-025-01110-z","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
N-type Ca2+ channels mediate the stimuli-dependent α-synuclein secretion in mouse striatum.
The secretion of α-synuclein from presynaptic terminals is controlled by neuronal activity through a calcium-dependent mechanism. To address the role of voltage gated calcium channels in this process, we used reverse brain microdialysis to monitor α-synuclein release in vivo in the presence of selective channel inhibitors. Our results revealed that the ω-conotoxin GVIA-sensitive N-type calcium channels are the major mediators of stimulated α-synuclein secretion in mouse striatum.
期刊介绍:
npj Parkinson's Disease is a comprehensive open access journal that covers a wide range of research areas related to Parkinson's disease. It publishes original studies in basic science, translational research, and clinical investigations. The journal is dedicated to advancing our understanding of Parkinson's disease by exploring various aspects such as anatomy, etiology, genetics, cellular and molecular physiology, neurophysiology, epidemiology, and therapeutic development. By providing free and immediate access to the scientific and Parkinson's disease community, npj Parkinson's Disease promotes collaboration and knowledge sharing among researchers and healthcare professionals.