D2 receptor antagonist raclopride regulates glutamatergic neuronal activity in the pedunculopontine nucleus in a rat model of Parkinson's disease

Biomedical Technology Pub Date : 2024-10-25 DOI:10.1016/j.bmt.2024.10.002

Hongli Chang , Bo Liu , Hongguang Chang , Na Li , Min Xu , Guilai Zuo , Wubing He , Xuenan Wang

{"title":"D2 receptor antagonist raclopride regulates glutamatergic neuronal activity in the pedunculopontine nucleus in a rat model of Parkinson's disease","authors":"Hongli Chang , Bo Liu , Hongguang Chang , Na Li , Min Xu , Guilai Zuo , Wubing He , Xuenan Wang","doi":"10.1016/j.bmt.2024.10.002","DOIUrl":null,"url":null,"abstract":"<div><div>Parkinson disease (PD) is defined by the loss of dopamine (DA). Changes in the pedunculopontine nucleus (PPN), particularly in local field potential (LFP), can be attributed to deficits in DA and DA receptor expression levels. PPN is a heterogeneous nucleus consisting of cholinergic, γ-aminobutyric acid (GABAergic), and glutamatergic neurons. However, it is unclear whether low levels of DA receptors affect the activity of different PPN neuron types. We record the neuronal activity of PPN by administering the selective dopamine D1 and D2 receptor antagonists, SCH23390 and Raclopride, respectively. This study discover that the firing rates of glutamatergic neurons could be normalized, and their firing patterns were more consistent in lesioned rats treated with raclopride. Raclopride administration could correct the increased coherence and phase locking between glutamatergic spikes and beta-band oscillatory activity in lesioned rats. Raclopride administration correct the increased coherence and phase locking between glutamatergic spikes and beta-band oscillatory activity in lesioned rats.</div></div>","PeriodicalId":100180,"journal":{"name":"Biomedical Technology","volume":"8 ","pages":"Pages 81-91"},"PeriodicalIF":0.0000,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedical Technology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2949723X24000321","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Parkinson disease (PD) is defined by the loss of dopamine (DA). Changes in the pedunculopontine nucleus (PPN), particularly in local field potential (LFP), can be attributed to deficits in DA and DA receptor expression levels. PPN is a heterogeneous nucleus consisting of cholinergic, γ-aminobutyric acid (GABAergic), and glutamatergic neurons. However, it is unclear whether low levels of DA receptors affect the activity of different PPN neuron types. We record the neuronal activity of PPN by administering the selective dopamine D1 and D2 receptor antagonists, SCH23390 and Raclopride, respectively. This study discover that the firing rates of glutamatergic neurons could be normalized, and their firing patterns were more consistent in lesioned rats treated with raclopride. Raclopride administration could correct the increased coherence and phase locking between glutamatergic spikes and beta-band oscillatory activity in lesioned rats. Raclopride administration correct the increased coherence and phase locking between glutamatergic spikes and beta-band oscillatory activity in lesioned rats.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

在帕金森病大鼠模型中，D2 受体拮抗剂拉克必利可调节足底核的谷氨酸能神经元活动

帕金森病（PD）的定义是多巴胺（DA）的丧失。足底核（PPN）的变化，尤其是局部场电位（LFP）的变化，可归因于 DA 和 DA 受体表达水平的缺陷。PPN 是一个由胆碱能、γ-氨基丁酸（GABA）能和谷氨酸能神经元组成的异质性核团。然而，目前还不清楚低水平的 DA 受体是否会影响不同类型 PPN 神经元的活动。我们分别使用选择性多巴胺 D1 和 D2 受体拮抗剂 SCH23390 和 Raclopride 记录 PPN 神经元的活动。研究发现，使用拉氯必利治疗的病变大鼠谷氨酸能神经元的发射率可恢复正常，其发射模式也更加一致。服用拉氯必利可纠正病变大鼠谷氨酸能尖峰与β波段振荡活动之间增加的一致性和锁相。服用拉氯必利可纠正病变大鼠谷氨酸能尖峰与β波段振荡活动之间增加的相干性和锁相。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Biomedical Technology

CiteScore

4.10

自引率

0.00%

发文量