Drebrin immunoreactivity in the striatum of a rat model of levodopa-induced dyskinesia.
Drebrin immunoreactivity in the striatum of a rat model of levodopa-induced dyskinesia.
复制标题
左旋多巴诱导的运动障碍大鼠模型纹状体中的 Drebrin 免疫反应性。
DOI：
10.1111/neup.12009
复制
发表时间：
2013
期刊：
影响因子：
2.3
通讯作者：
Tomiyama M.
中科院分区：
文献类型：
--
作者：
Nishijima H;Arai A;Kimura T;Mori F;Yamada J;Migita K;Wakabayashi K;Baba M;Ueno S;Tomiyama M.
左旋多巴诱导的运动障碍被认为是由皮质纹状体突触的适应不良可塑性引起的。突触可塑性基于树突棘的形态变化。为了阐明左旋多巴诱导的运动障碍大鼠模型的纹状体中是否发生了棘的形态学变化，我们使用左旋多巴重复治疗的6-羟基多巴胺损伤大鼠，检测了位于兴奋性突触树突棘的肌动蛋白结合蛋白dreplatin的免疫反应性。在左旋多巴诱导的运动障碍模型的多巴胺去神经纹状体中，多巴胺免疫反应性细胞器（假定的棘）的横截面积大于帕金森病模型的横截面积。免疫电子显微镜检查证实，在左旋多巴诱导的运动障碍模型的去多巴胺神经支配的纹状体中，drebrin免疫反应性棘变大，但在帕金森病模型中则不然。这些结果表明，左旋多巴诱导的运动障碍的发生与皮质纹状体兴奋性突触处树突棘的增大有关。
Levodopa‐induced dyskinesia has been suggested to result from maladaptive plasticity at corticostriatal synapses. Synaptic plasticity is based upon morphologic changes of dendritic spines. To elucidate whether the morphologic changes of spines occur in the striatum of rat models of levodopa‐induced dyskinesia, we examined immunoreactivity of drebrin, an actin‐binding protein localized in dendritic spines of excitatory synapses, using 6‐hydroxydopamine‐lesioned rats repeatedly treated with levodopa. The cross‐sectional area of drebrin‐immunoreactive organelles, putative spines, in the dopamine‐denervated striatum of the levodopa‐induced dyskinesia model was greater than that of the Parkinson's disease model. Immunoelectron microscopic examinations confirmed that drebrin‐immunoreactive spines became enlarged in the dopamine‐denervated striatum of the levodopa‐induced dyskinesia model, but not in the Parkinson's disease model. These results suggest that the development of levodopa‐induced dyskinesia is associated with enlargement of dendritic spines at corticostriatal excitatory synapses.