Pathogenesis of levodopa-induced dyskinesia:: focus on D1 and D3 dopamine receptors
Pathogenesis of levodopa-induced dyskinesia:: focus on D1 and D3 dopamine receptors
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DOI：
10.1016/j.parkreldis.2004.11.005
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发表时间：
2005-06-01
影响因子：
4.1
通讯作者：
Bezard, E
中科院分区：
文献类型：
--
作者：
Guigoni, C;Aubert, I;Bezard, E
不自主运动或运动障碍是左旋多巴治疗帕金森病的一种使人衰弱的并发症。利用猴脑银行构成的左旋多巴诱导的运动障碍的病理生理学研究，我们在这里报告的变化影响D1，D2和D3多巴胺受体的纹状体内的四个实验组的非人类灵长类动物：正常，帕金森病。用左旋多巴治疗的帕金森病患者，不伴有或伴有运动障碍。我们还报告了抑制蛋白和G蛋白偶联受体激酶的可能作用。(C)2005爱思唯尔有限公司保留所有权利。
Involuntary movements, or dyskinesia, represent a debilitating complication of levodopa therapy for Parkinson's disease. Taking advantage of a monkey brain bank constituted to study the pathophysiology of levodopa-induced dyskinesia, we here report the changes affecting D1, D2 and D3 dopamine receptors within the striatum of four experimental groups of non-human primates: normal, parkinsonian. parkinsonian treated with levodopa without or with dyskinesia. We also report the possible role of arrestin and G protein-coupled receptor kinases. (C) 2005 Elsevier Ltd. All rights reserved.