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帕金森病患者皮质对丘脑底核神经元驱动的时空动力学。

Spatio-temporal dynamics of cortical drive to human subthalamic nucleus neurons in Parkinson's disease.

机构信息

MRC Brain Network Dynamics Unit, Dept. of Pharmacology, University of Oxford, Oxford OX1 3TH, United Kingdom; Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.

Department of Neurophysiology and Pathophysiology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.

出版信息

Neurobiol Dis. 2018 Apr;112:49-62. doi: 10.1016/j.nbd.2018.01.001. Epub 2018 Jan 4.

DOI:10.1016/j.nbd.2018.01.001
PMID:29307661
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5821899/
Abstract

Pathological synchronisation of beta frequency (12-35Hz) oscillations between the subthalamic nucleus (STN) and cerebral cortex is thought to contribute to motor impairment in Parkinson's disease (PD). For this cortico-subthalamic oscillatory drive to be mechanistically important, it must influence the firing of STN neurons and, consequently, their downstream targets. Here, we examined the dynamics of synchronisation between STN LFPs and units with multiple cortical areas, measured using frontal ECoG, midline EEG and lateral EEG, during rest and movement. STN neurons lagged cortical signals recorded over midline (over premotor cortices) and frontal (over prefrontal cortices) with stable time delays, consistent with strong corticosubthalamic drive, and many neurons maintained these dynamics during movement. In contrast, most STN neurons desynchronised from lateral EEG signals (over primary motor cortices) during movement and those that did not had altered phase relations to the cortical signals. The strength of synchronisation between STN units and midline EEG in the high beta range (25-35Hz) correlated positively with the severity of akinetic-rigid motor symptoms across patients. Together, these results suggest that sustained synchronisation of STN neurons to premotor-cortical beta oscillations play an important role in disrupting the normal coding of movement in PD.

摘要

丘脑底核(STN)和大脑皮层之间的β频率(12-35Hz)振荡的病理性同步被认为有助于帕金森病(PD)的运动障碍。为了使皮质-丘脑底核的振荡驱动具有机制上的重要性,它必须影响 STN 神经元的放电,从而影响它们的下游靶点。在这里,我们研究了使用额 ECoG、中线 EEG 和外侧 EEG 测量的 STN LFPs 与来自多个皮质区域的单位之间在休息和运动期间的同步动力学。STN 神经元与中线(运动前皮质)和额部(前额叶皮质)记录的皮质信号滞后,具有稳定的时间延迟,这与强烈的皮质-丘脑底核驱动一致,并且许多神经元在运动期间保持这些动力学。相比之下,大多数 STN 神经元在运动期间与外侧 EEG 信号(初级运动皮质)去同步,而那些没有去同步的神经元与皮质信号的相位关系发生改变。STN 单元与中线 EEG 在高β范围内(25-35Hz)的同步强度与患者之间运动性无动性-僵硬运动症状的严重程度呈正相关。这些结果表明,STN 神经元对运动前皮质β振荡的持续同步在破坏 PD 中运动的正常编码方面起着重要作用。

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