Axial levodopa-induced dyskinesias and neuronal activity in the dorsal striatum.

Axial levodopa-induced dyskinesias and neuronal activity in the dorsal striatum.
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轴向左旋多巴引起的背纹状体和神经元活性。

DOI:
10.1016/j.neuroscience.2016.11.046
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发表时间:
2017-02-20
期刊:
影响因子:
3.3
通讯作者:
Narayanan NS
Narayanan NS
中科院分区:
医学3区
文献类型:
--
作者:
Alberico SL;Kim YC;Lence T;Narayanan NS

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左旋多巴引起的运动障碍是限制帕金森病治疗效果的异常不自主运动。虽然运动障碍涉及纹状体,但纹状体神经元如何参与运动障碍运动尚不清楚。在这里,我们记录在左旋多巴诱导的轴向运动障碍的小鼠纹状体神经元。我们开发了一个自动化的三维运动跟踪系统,以捕获轴向运动障碍的发展在~10 ms的分辨率,并将这些运动与纹状体中型多刺神经元和快速尖峰中间神经元的神经元活动。中棘神经元的平均放电频率随着轴向运动障碍的发展而增加,并且中棘神经元和快速尖峰中间神经元都在轴向运动障碍周围受到调制。我们还发现,在运动障碍的纹状体中,δ场电位功率增加,并且这种增加的δ功率与纹状体神经元相结合。我们的研究结果提供了深入了解纹状体网络如何改变左旋多巴诱导的运动障碍的发展,并建议增加中棘神经元放电,增加三角洲场电位功率,和异常三角洲耦合可能是运动障碍的神经生理学特征。这些数据可能有助于了解纹状体在帕金森病运动障碍发病机制中的作用。
Levodopa-induced dyskinesias are abnormal involuntary movements that limit the effectiveness of treatments for Parkinson’s disease. Although dyskinesias involve the striatum, it is unclear how striatal neurons are involved in dyskinetic movements. Here we record from striatal neurons in mice during levodopa-induced axial dyskinesias. We developed an automated 3-dimensional motion tracking system to capture the development of axial dyskinesias at ~10 ms resolution, and correlated these movements with neuronal activity of striatal medium spiny neurons and fast spiking interneurons. The average firing rate of medium spiny neurons increased as axial dyskinesias developed, and both medium spiny neurons and fast spiking interneurons were modulated around axial dyskinesias. We also found that delta field potential power increased in the striatum with dyskinesia, and that this increased delta power coupled with striatal neurons. Our findings provide insight into how striatal networks change as levodopa-induced dyskinesias develop, and suggest that increased medium spiny neuron firing, increased delta field potential power, and abnormal delta-coupling may be neurophysiological signatures of dyskinesias. These data could be helpful in understanding the role of the striatum in the pathogenesis of dyskinesias in Parkinson’s disease.