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帕金森病与多系统萎缩患者运动皮质可塑性的多巴胺调制差异。

Differences in dopaminergic modulation to motor cortical plasticity between Parkinson's disease and multiple system atrophy.

机构信息

Department of Neurology and Neuroscience, Nagoya City University Graduate School of Medical Science, Nagoya, Japan.

出版信息

PLoS One. 2013 May 3;8(5):e62515. doi: 10.1371/journal.pone.0062515. Print 2013.

Abstract

Dopamine modulates the synaptic plasticity in the primary motor cortex (M1). To evaluate whether the functioning of the cortico-striatal circuit is necessary for this modulation, we applied a paired associative stimulation (PAS) protocol that comprised an electric stimulus to the right median nerve at the wrist and subsequent transcranial magnetic stimulation of the left M1, to 10 patients with Parkinson's disease (PD) and 10 with multiple system atrophy of the parkinsonian type (MSA-P) with and without dopamine replacement therapy (-on/off). To investigate the M1 function, motor-evoked potentials (MEPs) were measured before and after the PAS. In both patient groups without medication, the PAS protocol failed to increase the averaged amplitude of MEPs. The dopamine replacement therapy in PD, but not in MSA-P effectively restored the PAS-induced MEP increase. This suggests that not the existence of dopamine itself but the activation of cortico-striatal circuit might play an important role for cortical plasticity in the human M1.

摘要

多巴胺调节初级运动皮层(M1)的突触可塑性。为了评估皮质纹状体回路的功能对于这种调节是否必要,我们应用了一种配对关联刺激(PAS)方案,包括在手腕处对右侧正中神经施加电刺激,随后对左侧 M1 进行经颅磁刺激,对 10 名帕金森病(PD)患者和 10 名多系统萎缩帕金森型(MSA-P)患者进行了研究,这些患者在多巴胺替代治疗(ON/OFF)期间进行了此项研究。为了研究 M1 功能,在 PAS 前后测量了运动诱发电位(MEP)。在没有药物治疗的两组患者中,PAS 方案均未能增加 MEP 的平均幅度。PD 中的多巴胺替代治疗,但 MSA-P 中无效,有效地恢复了 PAS 诱导的 MEP 增加。这表明,不是多巴胺本身的存在,而是皮质纹状体回路的激活可能在人类 M1 的皮质可塑性中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f5ac/3643922/d9553473df7a/pone.0062515.g001.jpg

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