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帕金森病运动迟缓的神经网络模型。

A neural network model of Parkinson's disease bradykinesia.

作者信息

Cutsuridis Vassilis, Perantonis Stavros

机构信息

Computational Intelligence Laboratory, Institute of Informatics and Telecommunications, National Center for Scientific Research 'Demokritos', Agia Paraskevi, Athens GR-15310, Greece.

出版信息

Neural Netw. 2006 May;19(4):354-74. doi: 10.1016/j.neunet.2005.08.016. Epub 2005 Dec 13.

Abstract

Parkinson's disease (PD) is caused by dopamine (DA) depletion consequent to cell degeneration in the substantia nigra pars compacta (SNc) and the ventral tegmental area (VTA). Although computational analyses of PD have focused on DA depletion in DA-recipient parts of the basal ganglia, there is also extensive DAergic innervation of the frontal and parietal cortex as well as the spinal cord. To understand PD bradykinesia, a comprehensive network model is needed to study how patterns of DA depletion at key cellular sites in the basal ganglia, cortex and spinal cord contribute to disordered neuronal and spinal cord activity and other PD symptoms. We extend a basal ganglia-cortico-spinal circuit for control of voluntary arm movements by incorporating DAergic innervation of cells in the cortical and spinal components of the circuit. The resultant model simulates successfully several of the main reported effects of DA depletion on neuronal, electromyographic (EMG), and movement parameters of PD bradykinesia.

摘要

帕金森病(PD)是由黑质致密部(SNc)和腹侧被盖区(VTA)的细胞变性导致多巴胺(DA)耗竭引起的。尽管对PD的计算分析主要集中在基底神经节DA接受部位的DA耗竭,但额叶和顶叶皮质以及脊髓也有广泛的多巴胺能神经支配。为了理解PD运动迟缓,需要一个综合网络模型来研究基底神经节、皮质和脊髓关键细胞部位的DA耗竭模式如何导致神经元和脊髓活动紊乱以及其他PD症状。我们通过纳入该回路皮质和脊髓成分中细胞的多巴胺能神经支配,扩展了一个用于控制自愿手臂运动的基底神经节 - 皮质 - 脊髓回路。所得模型成功模拟了DA耗竭对PD运动迟缓的神经元、肌电图(EMG)和运动参数的几种主要报道效应。

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