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首页> 外文期刊>The European Journal of Neuroscience >Dopamine depletion increases the power and coherence of beta-oscillations in the cerebral cortex and subthalamic nucleus of the awake rat.
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Dopamine depletion increases the power and coherence of beta-oscillations in the cerebral cortex and subthalamic nucleus of the awake rat.

机译：多巴胺的消耗增加了清醒大鼠大脑皮层和丘脑底核中β-振荡的能力和相干性。

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Abstract Local field potentials (LFPs) recorded from the subthalamic nucleus (STN) of untreated patients implanted with stimulation electrodes for the treatment of Parkinson's disease (PD) demonstrate strong coherence with the cortical electroencephalogram over the beta-frequency range (15-30 Hz). However, studies in animal models of PD emphasize increased temporal coupling in cortico-basal ganglia circuits at substantially lower frequencies, undermining the potential usefulness of these models. Here we show that 6-hydroxydopamine (6-OHDA) lesions of midbrain dopamine neurons are associated with significant increases in the power and coherence of beta-frequency oscillatory activity present in LFPs recorded from frontal cortex and STN of awake rats, as compared with the healthy animal. Thus, the pattern of synchronization between population activity in the STN and cortex in the 6-OHDA-lesioned rodent model of PD closely parallels that seen in the parkinsonian human. The peak frequency of coherent activity in the beta-frequency range was increased in lesioned animals during periods of spontaneous and sustained movement. Furthermore, administration of the dopamine receptor agonist apomorphine to lesioned animals suppressed beta-frequency oscillations, and increased coherent activity at higher frequencies in the cortex and STN, before producing the rotational behaviour indicative of successful lesion. Taken together, these results support a crucial role for dopamine in the modulation of population activity in cortico-basal ganglia circuits, whereby dopaminergic mechanisms effectively filter out synchronized, rhythmic activity at beta-frequencies at the systems level, and shift temporal couplings in these circuits to higher frequencies. These changes may be important in regulating movement.
机译：摘要未经治疗的植入刺激电极治疗帕金森氏病（PD）的患者的丘脑下丘脑核（STN）记录的局部场电势（LFP）在β频率范围（15-30 Hz）上与皮层脑电图表现出强相干性。但是，PD动物模型的研究强调，皮质-基底神经节回路在明显较低的频率下会增加时间耦合，从而破坏了这些模型的潜在实用性。在这里，我们显示中脑多巴胺神经元的6-羟基多巴胺（6-OHDA）损伤与清醒大鼠额叶皮层和STN记录的LFPs中存在的β-频率振荡活性的功率和相干性显着增加相关，而与健康的动物。因此，在PD的6-OHDA损伤的啮齿动物模型中，STN中的种群活动与皮层之间的同步模式与帕金森氏症中的相似。在自发性和持续性运动期间，病变动物的相干活动的峰值频率在β频率范围内增加。此外，在产生指示成功病变的旋转行为之前，向患病动物施用多巴胺受体激动剂阿扑吗啡可抑制β频率振荡，并在较高的皮层和STN频率下增强相干活性。综上所述，这些结果支持多巴胺在调节皮质-基底神经节回路中的种群活动中起关键作用，从而多巴胺能机制有效过滤掉系统级处于β频率的同步节律活动，并改变这些回路中的时间耦合到更高的频率。这些变化对于调节运动可能很重要。

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