| 常晓赞葛顺楠杨晨李敏井晓容朱俊玲王学廉△ 高国栋△.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[J].,2011,11(10):1813-1816 |
| 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 |
| Abnormalities of EcoG and Field Potential of Basal Ganglia in6-OHDA-lesioned Rats with Parkinson's Disease during Rapid EyeMovement Sleep |
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| DOI： |
| 中文关键词: 帕金森病 大鼠 快动眼睡眠 皮层脑电 基底节场电位 |
| 英文关键词: Parkinson disease Rat Rapid eye movement sleep Electrocorticogram motor cortex |
| 基金项目:国家自然科学基金重点项目（30930095） |
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| 中文摘要: |
| 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同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θ 和γ 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。 |
| 英文摘要: |
| Objective: 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 sleep behavior disorder of PD. |
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