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The role of coupling connections in a model of the cortico-basal ganglia-thalamocortical neural loop for the generation of beta oscillations.
Neural Networks ( IF 6.0 ) Pub Date : 2019-12-30 , DOI: 10.1016/j.neunet.2019.12.021
Chen Liu 1 , Changsong Zhou 2 , Jiang Wang 3 , Chris Fietkiewicz 4 , Kenneth A Loparo 4
Affiliation  

Excessive neural synchronization in the cortico-basal ganglia-thalamocortical circuits in the beta (β) frequency range (12-35 Hz) is closely associated with dopamine depletion in Parkinson's disease (PD) and correlated with movement impairments, but the neural basis remains unclear. In this work, we establish a double-oscillator neural mass model for the cortico-basal ganglia-thalamocortical closed-loop system and explore the impacts of dopamine depletion induced changes in coupling connections within or between the two oscillators on neural activities within the loop. Spectral analysis of the neural mass activities revealed that the power and frequency of their principal components are greatly dependent on the coupling strengths between nuclei. We found that the increased intra-coupling in the basal ganglia-thalamic (BG-Th) oscillator contributes to increased oscillations in the lower β frequency band (12-25 Hz), while increased intra-coupling in the cortical oscillator mainly contributes to increased oscillations in the upper β frequency band (26-35 Hz). Interestingly, pathological upper β oscillations in the cortical oscillator may be another origin of the lower β oscillations in the BG-Th oscillator, in addition to increased intra-coupling strength within the BG-Th network. Lower β oscillations in the BG-Th oscillator can also change the dominant oscillation frequency of a cortical nucleus from the upper to the lower β band. Thus, this work may pave the way towards revealing a possible neural basis underlying the Parkinsonian state.

中文翻译:

耦合连接在皮质基底神经节-丘脑皮质神经环路模型中的作用,用于产生β振荡。

在β(β)频率范围(12-35 Hz)的皮质基底神经节-丘脑皮质回路中过度的神经同步与帕金森病(PD)中的多巴胺消耗密切相关且与运动障碍相关,但神经基础尚不清楚。在这项工作中,我们为皮质基底神经节-丘脑皮质闭环系统建立了一个双振荡神经质量模型,并探讨了多巴胺耗竭引起的两个振荡器内部或之间的耦合连接变化对环路内神经活动的影响。对神经质量活动的频谱分析表明,其主要成分的功率和频率在很大程度上取决于原子核之间的耦合强度。我们发现基底神经节-丘脑(BG-Th)振荡器中的内部耦合增加有助于在较低的β频带(12-25 Hz)中增加振荡,而皮质振荡器中的内部耦合增加则主要有助于增大在较高的β频段(26-35 Hz)中产生振荡。有趣的是,除了增加BG-Th网络内的内部耦合强度外,皮质振荡器中的病理性高β振荡可能是BG-Th振荡器中低β振荡的另一个起源。BG-Th振荡器中的较低β振荡也可以将皮质核的主要振荡频率从较高β频带改变为较低β频带。因此,这项工作可能为揭示潜在的帕金森状态的神经基础铺平了道路。
更新日期:2019-12-30
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