右侧额下回作为基底神经节-丘脑皮质反应抑制回路的关键节点和有效调节器

Qian Zhuang, Lei Qiao, Lei Xu, Shuxia Yao, Shuaiyu Chen, Xiaoxiao Zheng, Jialin Li, Meina Fu, Keshuang Li, Deniz Vatansever, Stefania Ferraro, Keith M Kendrick, Benjamin Becker
{"title":"右侧额下回作为基底神经节-丘脑皮质反应抑制回路的关键节点和有效调节器","authors":"Qian Zhuang, Lei Qiao, Lei Xu, Shuxia Yao, Shuaiyu Chen, Xiaoxiao Zheng, Jialin Li, Meina Fu, Keshuang Li, Deniz Vatansever, Stefania Ferraro, Keith M Kendrick, Benjamin Becker","doi":"10.1093/psyrad/kkad016","DOIUrl":null,"url":null,"abstract":"Abstract Background The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models. However, the pivotal nodes and directed casual regulation within this inhibitory circuit in humans remains controversial. Methods Here, we capitalize on the recent progress in robust and biologically plausible directed causal modelling (DCM-PEB) and a large response inhibition dataset (n=250) acquired with concomitant functional fMRI to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP) and thalamus (rThal). Results The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model. Conclusions Together these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.","PeriodicalId":93496,"journal":{"name":"Psychoradiology","volume":"32 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"The right inferior frontal gyrus as pivotal node and effective regulator of the basal ganglia-thalamocortical response inhibition circuit\",\"authors\":\"Qian Zhuang, Lei Qiao, Lei Xu, Shuxia Yao, Shuaiyu Chen, Xiaoxiao Zheng, Jialin Li, Meina Fu, Keshuang Li, Deniz Vatansever, Stefania Ferraro, Keith M Kendrick, Benjamin Becker\",\"doi\":\"10.1093/psyrad/kkad016\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Abstract Background The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models. However, the pivotal nodes and directed casual regulation within this inhibitory circuit in humans remains controversial. Methods Here, we capitalize on the recent progress in robust and biologically plausible directed causal modelling (DCM-PEB) and a large response inhibition dataset (n=250) acquired with concomitant functional fMRI to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP) and thalamus (rThal). Results The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model. Conclusions Together these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.\",\"PeriodicalId\":93496,\"journal\":{\"name\":\"Psychoradiology\",\"volume\":\"32 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Psychoradiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1093/psyrad/kkad016\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Psychoradiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/psyrad/kkad016","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

摘要

背景:在动物模型中,特定的基底神经节-丘脑皮质回路参与反应抑制已被广泛绘制。然而,这一抑制回路中的关键节点和定向随意调节在人类中仍然存在争议。在此,我们利用鲁棒性和生物学上合理的定向因果模型(DCM-PEB)的最新进展,以及通过功能磁共振成像获得的大型反应抑制数据集(n=250)来确定关键节点,它们通过生物变量(性别)和抑制回路中的抑制表现进行因果调节和调节,抑制回路包括右额下回(rIFG)、尾状核(rCau)、白球(rGP)和丘脑(rThal)。结果整个神经回路表现出高度的内在连通性,反应抑制极大地增加了从rIFG到rCau和rThal的因果投射。直接比较进一步表明,反应抑制诱导了rIFG流入的增加,并增加了该区域对rCau和rThal的因果调节。此外,性别和表现会影响调节回路的结构,例如女性表现出增强的rThal自我抑制和减少的rThal对GP调制,而更好的抑制表现与更强的rThal与rIFG通信相关。此外,对照分析在左侧化模型中没有发现类似的关键通信。综上所述,这些发现表明了rIFG作为皮层下反应抑制节点的输入和因果调节的关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The right inferior frontal gyrus as pivotal node and effective regulator of the basal ganglia-thalamocortical response inhibition circuit
Abstract Background The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models. However, the pivotal nodes and directed casual regulation within this inhibitory circuit in humans remains controversial. Methods Here, we capitalize on the recent progress in robust and biologically plausible directed causal modelling (DCM-PEB) and a large response inhibition dataset (n=250) acquired with concomitant functional fMRI to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP) and thalamus (rThal). Results The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model. Conclusions Together these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.
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
CiteScore
2.50
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信