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运动在长期基底节变化中的作用:对异常运动反应的影响。

Role of movement in long-term basal ganglia changes: implications for abnormal motor responses.

机构信息

1Section of Neuropsychopharmacology, Department of Biomedical Sciences, University of Cagliari Cagliari, Italy.

出版信息

Front Comput Neurosci. 2013 Oct 23;7:142. doi: 10.3389/fncom.2013.00142.

DOI:10.3389/fncom.2013.00142
PMID:24167489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3805948/
Abstract

Abnormal involuntary movements (AIMs) and dyskinesias elicited by drugs that stimulate dopamine receptors in the basal ganglia are a major issue in the management of Parkinson's disease (PD). Preclinical studies in dopamine-denervated animals have contributed to the modeling of these abnormal movements, but the precise neurochemical and functional mechanisms underlying these untoward effects are still elusive. It has recently been suggested that the performance of movement may itself promote the later emergence of drug-induced motor complications, by favoring the generation of aberrant motor memories in the dopamine-denervated basal ganglia. Our recent results from hemiparkinsonian rats subjected to the priming model of dopaminergic stimulation are in agreement with this. These results demonstrate that early performance of movement is crucial for the manifestation of sensitized rotational behavior, indicative of an abnormal motor response, and neurochemical modifications in selected striatal neurons following a dopaminergic challenge. Building on this evidence, this paper discusses the possible role of movement performance in drug-induced motor complications, with a look at the implications for PD management.

摘要

异常不自主运动(AIMs)和由刺激基底神经节多巴胺受体的药物引起的运动障碍是帕金森病(PD)管理中的一个主要问题。在多巴胺去神经的动物中的临床前研究有助于对这些异常运动进行建模,但这些不良影响的确切神经化学和功能机制仍然难以捉摸。最近有人提出,运动本身可能通过促进多巴胺能去神经基底神经节中异常运动记忆的产生,从而促进药物引起的运动并发症的后期出现。我们最近对接受多巴胺刺激引发模型的偏侧帕金森病大鼠的研究结果与这一观点一致。这些结果表明,运动的早期表现对于表现出敏感的旋转行为(表明异常运动反应)以及多巴胺能挑战后选定纹状体神经元的神经化学修饰至关重要。基于这一证据,本文讨论了运动表现在药物引起的运动并发症中的可能作用,并探讨了对 PD 管理的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ec9/3805948/dab518beb894/fncom-07-00142-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ec9/3805948/3a85fc3824e6/fncom-07-00142-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ec9/3805948/dab518beb894/fncom-07-00142-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ec9/3805948/3a85fc3824e6/fncom-07-00142-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ec9/3805948/dab518beb894/fncom-07-00142-g0002.jpg

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2
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Exp Neurol. 2013 Sep;247:663-72. doi: 10.1016/j.expneurol.2013.03.002. Epub 2013 Mar 13.
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NeuroRehabilitation. 2012;30(4):295-301. doi: 10.3233/NRE-2012-0758.
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