半帕金森小鼠脑切片皮层β振荡。

IF 2.5 4区医学 Q3 NEUROSCIENCES

Neuroscience Letters Pub Date : 2025-01-18 DOI:10.1016/j.neulet.2025.138128

Aidán Ortega , Antonio Laville , Montserrat Padilla-Orozco , Yohana Parrado , Dagoberto Tapia , Miguel Serrano-Reyes , Janintzitzic López-Niño , Héctor A. Vázquez-Vázquez , Elvira Galarraga , José Bargas

{"title":"半帕金森小鼠脑切片皮层β振荡。","authors":"Aidán Ortega , Antonio Laville , Montserrat Padilla-Orozco , Yohana Parrado , Dagoberto Tapia , Miguel Serrano-Reyes , Janintzitzic López-Niño , Héctor A. Vázquez-Vázquez , Elvira Galarraga , José Bargas","doi":"10.1016/j.neulet.2025.138128","DOIUrl":null,"url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to significant motor and non-motor symptoms. Beta oscillations in cortical areas are a pathognomonic sign. Here we ask whether these oscillations can be recorded in <em>in vitro</em> cortical tissue despite severing the cortico-basal ganglia-thalamo-cortical loop. M1/M2 cortex of hemi parkinsonian mice (6-OHDA) was recorded with multielectrode arrays (MEAs). Spectral decomposition analysis shows a significantly augmented beta band power with respect to controls. The administration of L-DOPA diminished this exacerbated beta rhythm. This result suggests that plastic changes induced by dopamine (DA) depletion remain in isolated cortical tissue even when the complete circuit is no longer present. This finding brings the opportunity to test anti-parkinsonian drugs <em>in vitro</em> by quantifying cortical beta band power.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"849 ","pages":"Article 138128"},"PeriodicalIF":2.5000,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cortical beta oscillation in brain slices of hemi parkinsonian mice\",\"authors\":\"Aidán Ortega , Antonio Laville , Montserrat Padilla-Orozco , Yohana Parrado , Dagoberto Tapia , Miguel Serrano-Reyes , Janintzitzic López-Niño , Héctor A. Vázquez-Vázquez , Elvira Galarraga , José Bargas\",\"doi\":\"10.1016/j.neulet.2025.138128\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to significant motor and non-motor symptoms. Beta oscillations in cortical areas are a pathognomonic sign. Here we ask whether these oscillations can be recorded in <em>in vitro</em> cortical tissue despite severing the cortico-basal ganglia-thalamo-cortical loop. M1/M2 cortex of hemi parkinsonian mice (6-OHDA) was recorded with multielectrode arrays (MEAs). Spectral decomposition analysis shows a significantly augmented beta band power with respect to controls. The administration of L-DOPA diminished this exacerbated beta rhythm. This result suggests that plastic changes induced by dopamine (DA) depletion remain in isolated cortical tissue even when the complete circuit is no longer present. This finding brings the opportunity to test anti-parkinsonian drugs <em>in vitro</em> by quantifying cortical beta band power.</div></div>\",\"PeriodicalId\":19290,\"journal\":{\"name\":\"Neuroscience Letters\",\"volume\":\"849 \",\"pages\":\"Article 138128\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-01-18\",\"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/S0304394025000163\",\"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/S0304394025000163","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 0

摘要

帕金森病（PD）是一种神经退行性疾病，其特征是黑质致密部多巴胺能神经元的进行性丧失，导致明显的运动和非运动症状。皮层区域的β振荡是一种病征。在这里，我们询问这些振荡是否可以在体外皮层组织中记录，尽管切断了皮质-基底神经节-丘脑-皮层回路。采用多电极阵列（MEAs）对半帕金森小鼠M1/M2皮质（6-OHDA）进行记录。光谱分解分析表明，相对于控制，显著增加β波段功率。左旋多巴的使用减少了这种加剧的β节律。这一结果表明，多巴胺（DA）耗竭引起的可塑性变化在孤立的皮质组织中仍然存在，即使完整的回路不再存在。这一发现为通过量化皮质β带功率来测试抗帕金森病药物的体外测试提供了机会。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Cortical beta oscillation in brain slices of hemi parkinsonian mice

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic neurons in the substantia nigra pars compacta, leading to significant motor and non-motor symptoms. Beta oscillations in cortical areas are a pathognomonic sign. Here we ask whether these oscillations can be recorded in in vitro cortical tissue despite severing the cortico-basal ganglia-thalamo-cortical loop. M1/M2 cortex of hemi parkinsonian mice (6-OHDA) was recorded with multielectrode arrays (MEAs). Spectral decomposition analysis shows a significantly augmented beta band power with respect to controls. The administration of L-DOPA diminished this exacerbated beta rhythm. This result suggests that plastic changes induced by dopamine (DA) depletion remain in isolated cortical tissue even when the complete circuit is no longer present. This finding brings the opportunity to test anti-parkinsonian drugs in vitro by quantifying cortical beta band power.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Neuroscience Letters 医学-神经科学

CiteScore

5.20

自引率

0.00%

发文量

408

审稿时长

50 days

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.