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首页> 外文期刊>Journal of Neurophysiology >Effects of high-frequency stimulation of the internal pallidal segment on neuronal activity in the thalamus in parkinsonian monkeys
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Effects of high-frequency stimulation of the internal pallidal segment on neuronal activity in the thalamus in parkinsonian monkeys

机译:高频刺激内苍白节对帕金森病猴丘脑神经元活性的影响

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Deep brain stimulation of the internal globus pallidus (GPi) is a major treatment for advanced Parkinson’s disease. The effects of this intervention on electrical activity patterns in targets of GPi output, specifically in the thalamus, are poorly understood. The experiments described here examined these effects using electrophysiological recordings in two Rhesus monkeys rendered moderately parkinsonian through treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), after sampling control data in the same animals. Analysis of spontaneous spiking activity of neurons in the basal ganglia-receiving areas of the ventral thalamus showed that MPTP-induced parkinsonism is associated with a reduction of firing rates of segments of the data that contained neither bursts nor decelerations, and with increased burst firing. Spectral analyses revealed an increase of power in the 3-to 13-Hz band and a reduction in the γ-range in the spiking activity of these neurons. Electrical stimulation of the ventrolateral motor territory of GPi with macroelectrodes, mimicking deep brain stimulation in parkinsonian patients (bipolar electrodes, 0.5 mm intercontact distance, biphasic stimuli, 120 Hz, 100 μs/phase, 200 μA), had antiparkinsonian effects. The stimulation markedly reduced oscillations in thalamic firing in the 13-to 30-Hz range and uncoupled the spiking activity of recorded neurons from simultaneously recorded local field potential (LFP) activity. These results confirm that oscillatory and nonoscillatory characteristics of spontaneous activity in the basal ganglia receiving ventral thalamus are altered in MPTP-induced parkinsonism. Electrical stimulation of GPi did not entrain thalamic activity but changed oscillatory activity in the ventral thalamus and altered the relationship between spikes and simultaneously recorded LFPs.
机译:大脑内部苍白球(GPi)的深度大脑刺激是晚期帕金森氏病的主要治疗方法。这种干预对GPi输出目标(尤其是丘脑)中电活动模式的影响了解得很少。在对同一只动物的对照数据进行采样后,此处描述的实验使用电生理记录检查了两只恒河猴通过用1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)处理而产生帕金森氏症的效果。对腹侧丘脑基底神经节接收区神经元的自发尖峰活动的分析表明,MPTP诱发的帕金森氏症与既没有猝发也没有减速的数据段的触发率降低以及爆发触发的增加有关。频谱分析显示,这些神经元的3到13 Hz频段的功率增加,而γ范围的减小。用大电极电刺激GPi的腹侧运动区,模仿帕金森氏病患者的深部脑刺激(双极电极,0.5 mm的接触距离,双相刺激,120 Hz,100μs/相,200μA),具有抗帕金森病作用。刺激显着降低了丘脑放电在13至30 Hz范围内的振荡,并使已记录神经元的尖峰活动与同时记录的局部场电位(LFP)活动脱钩。这些结果证实,MPTP诱发的帕金森病改变了接受腹侧丘脑的基底神经节自发活动的振荡和非振荡特性。 GPi的电刺激并未引起丘脑活动,但改变了丘脑腹侧的振荡活动,并改变了峰值和同时记录的LFP之间的关系。

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