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右侧额下回和初级运动皮层的双位点β-经颅交流电刺激增强反应抑制:一项平行多对照与重复研究。

Dual-site beta tACS over rIFG and M1 enhances response inhibition: A parallel multiple control and replication study.

作者信息

Meng Qiujian, Zhu Ying, Yuan Ye, Ni Rui, Yang Li, Liu Jiafang, Bu Junjie

机构信息

Department of Intelligent Medical Engineering, School of Biomedical Engineering, Anhui Medical University, Hefei, China.

Department of Life Sciences, Imperial College London, London, United Kingdom.

出版信息

Int J Clin Health Psychol. 2023 Oct-Dec;23(4):100411. doi: 10.1016/j.ijchp.2023.100411. Epub 2023 Sep 14.

DOI:10.1016/j.ijchp.2023.100411
PMID:37731603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10507441/
Abstract

Response inhibition is a core component of cognitive control. Past electrophysiology and neuroimaging studies have identified beta oscillations and inhibitory control cortical regions correlated with response inhibition, including the right inferior frontal gyrus (rIFG) and primary motor cortex (M1). Hence, increasing beta activity in multiple brain regions is a potential way to enhance response inhibition. Here, a novel dual-site transcranial alternating current stimulation (tACS) method was used to modulate beta activity over the rIFG-M1 network in a sample of 115 (excluding 2 participants) with multiple control groups and a replicated experimental design. In Experiment 1, 70 healthy participants were randomly assigned to three dual-site beta-tACS groups, including in-phase, anti-phase or sham stimulation. During and after stimulation, participants were required to complete the stop-signal task, and electroencephalography (EEG) was collected before and after stimulation. The Barratt Impulsiveness Scale was completed before the experiment to evaluate participants' impulsiveness. In addition, we conducted an active control experiment with a sample size of 20 to exclude the potential effects of the dual-site tACS "return" electrode. To validate the behavioural findings of Experiment 1, 25 healthy participants took part in Experiment 2 and were randomized into two groups, including in-phase and sham stimulation groups. We found that compared to the sham group, in-phase but not anti-phase beta-tACS significantly improved both response inhibition performance and beta synchronization of the inhibitory control network in Experiment 1. Furthermore, the increased beta synchronization was correlated with enhanced response inhibition. In an independent sample of Experiment 2, the enhanced response inhibition performance observed in the in-phase group was replicated. After combining the data from the above two experiments, the time dynamics analysis revealed that the in-phase beta-tACS effect occurred in the post-stimulation period but not the stimulation period. The state-dependence analysis showed that individuals with poorer baseline response inhibition or higher attentional impulsiveness had greater improvement in response inhibition for the in-phase group. These findings strongly support that response inhibition in healthy adults can be improved by in-phase dual-site beta-tACS of the rIFG-M1 network, and provide a new potential treatment targets of synchronized cortical network activity for patients with clinically deficient response inhibition.

摘要

反应抑制是认知控制的核心组成部分。过去的电生理学和神经影像学研究已经确定了与反应抑制相关的β振荡和抑制控制皮层区域,包括右侧额下回(rIFG)和初级运动皮层(M1)。因此,增加多个脑区的β活动是增强反应抑制的一种潜在方法。在此,我们使用了一种新颖的双部位经颅交流电刺激(tACS)方法,在一个包含多个对照组和重复实验设计的115名参与者(不包括2名参与者)的样本中,调节rIFG-M1网络上的β活动。在实验1中,70名健康参与者被随机分配到三个双部位β-tACS组,包括同相、反相或假刺激组。在刺激期间和之后,参与者被要求完成停止信号任务,并在刺激前后收集脑电图(EEG)。在实验前完成巴拉特冲动性量表以评估参与者的冲动性。此外,我们进行了一个样本量为20的主动对照实验,以排除双部位tACS“返回”电极的潜在影响。为了验证实验1的行为学结果,25名健康参与者参加了实验2,并被随机分为两组,包括同相和假刺激组。我们发现,与假刺激组相比,在实验1中,同相而非反相的β-tACS显著提高了反应抑制性能和抑制控制网络的β同步性。此外,增加的β同步性与增强的反应抑制相关。在实验2的一个独立样本中,同相组中观察到的增强的反应抑制性能得到了重复。在合并上述两个实验的数据后,时间动态分析表明,同相β-tACS效应发生在刺激后时期而非刺激期。状态依赖性分析表明,基线反应抑制较差或注意力冲动性较高的个体,同相组的反应抑制改善更大。这些发现有力地支持了通过rIFG-M1网络的同相双部位β-tACS可以改善健康成年人的反应抑制,并为反应抑制临床缺陷的患者提供了一个同步皮层网络活动的新潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/570145edac29/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/70b40b7b467c/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/441c4369aafa/gr6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/570145edac29/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/70b40b7b467c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/974eb7ff0203/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/c3f2f87f1657/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/96e1feef7f80/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/03d40a7e3b8e/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/441c4369aafa/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/5d728a3161b5/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74a7/10507441/570145edac29/gr8.jpg

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