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Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation

机译:长期接受左旋多巴和烟碱样受体激动剂治疗的单侧多巴胺能神经支配总数近乎全的雌性小鼠运动障碍和脑源性神经营养因子水平

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摘要

BackgroundThe treatment of Parkinson’s disease is often complicated by levodopa-induced dyskinesia (LID). Nicotinic acetylcholine receptor agonists can alleviate LID in animal models but may be less effective in conditions of severe dopaminergic denervation. While the mechanisms of LID remain incompletely understood, elevated corticostriatal levels of the brain-derived neurotrophic factor (BDNF) have been suggested to play a role. Here, female mice with near-total unilateral 6-hydroxydopamine-induced nigrostriatal lesions were chronically treated with levodopa, and the effects of the α7 nicotinic receptor partial agonist AZD0328 and nicotine on LID were assessed. At the end of the experiment, BDNF protein levels in the prefrontal cortex and striatum were measured.
机译:背景帕金森氏病的治疗通常并发左旋多巴诱发的运动障碍(LID)。烟碱型乙酰胆碱受体激动剂可以减轻动物模型中的LID,但在严重多巴胺能神经支配的情况下效果可能较差。虽然对LID的机制仍未完全了解,但已提示大脑源性神经营养因子(BDNF)皮质皮质水平的升高起了作用。在这里,用左旋多巴对单侧6-羟基多巴胺诱导的黑纹状体病变近乎全部的雌性小鼠进行长期治疗,并评估α7烟碱样受体部分激动剂AZD0328和尼古丁对LID的影响。实验结束时,测量前额叶皮层和纹状体中的BDNF蛋白水平。

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