6-OHDA帕金森病大鼠快动眼睡眠状态下皮层脑电及基底节场电位的异常变化

目的：了解帕金森病（PD）模型大鼠在快动眼睡眠状态下皮层脑电和基底节场电位的异常变化。方法：用6-羟基多巴胺（6-OHDA）脑内两点注射法建立PD大鼠模型，并经阿扑吗啡注射诱发旋转对模型进行评价。通过多导宏电极在体电生理记录技术结合视频录像，对正常大鼠和6-OHDA大鼠PD模型进行苍白球场电位和皮层M1、M2区脑电的多部位24小时同时记录。功率谱分析和相干分析用于揭示快动眼睡眠状态下各记录位点信号的频率成分以及不N记录位点神经元集群之间的变化。结果：与正常大鼠相比，6-OHDA帕金森病模型大鼠在REM期间的皮层脑电在臼和y频段上都有变化：初级运动皮质M1区的θ频段成分消失，辅助运动区M2的θ频段成分略有增加，患侧苍白球的θ频段成分增大显著；M1区的γ频段成分增大，而γ频段成分在苍白球基本没有变化。结论：6-OHDA对中脑多巴胺能神经元的损害可造成大鼠双侧皮层M1区θ节律的消失和γ节律的增强，以及对侧M1-M2区之间在γ节律上的同步被显著增强，而γ节律在苍白球没有变化。这些异常电活动可能是由于VTA受损引起从而与帕金森病的快动眼睡眠行为障碍有关。

Abnormalities of EcoG and Field Potential of Basal Ganglia in 6-OHDA-lesioned Rats with Parkinson＇s Disease during Rapid Eye Movement Sleep

To investigate altered features of the electrocorticogram （ECoG） and local field potential of the globus pallidus of Parkinson disease （PD） rat models during rapid eye movement sleep （REM）. Methods： Sprague-Dawley rats with unilateral 6-hydroxydopamine （6-OHDA） lesions were used as the model of PD. Apomorphine induced contralateral rotations in PD rat models were examined to assure proper lesioning. Continuous video, local field potential （LFP） of the globus pallidus （GP）, Electrocorticogram （ECoG） of primary motor cortex （M1） and the secondary motor cortex （M2） were detected simultaneously for 24 hours or more. Power spectral densities （PSD） were computed to decompose distinct frequency components of signals recording at each electrode positions. Coherence analysis was used to assess the coupling or synchronization of brain activity between distributed neuronal populations at each electrode position. Results： Compared with the saline-treated rats, 6-OHDA-lesioned rats showed some differences during rapid eye movement sleep： rhythm in the ECoGs of primary motor cortex （M1） disappeared; rhythm in the ECoGs of the secondary motor cortex （M2） and rhythm in LFP of GP on the injected side increased; rhythm in the ECoGs of primary motor cortex （M 1） increased; rhythm in the LFP of GP did not change. Conclusion： 6-OHDA lesions of midbrain dopaminergic neurons of rat can induce the disappearance of rhythm and enhanced rhythm in the ECoGs of M1 and increase contralateral rhythm synchronization between the ECoGs of M1 and M2. These abnormal rhythms may be induced by the damage of ventra tegmental area （VTA） and have relationships with rapid eye movement sleeo behavior disorder of PD.