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首页> 外文期刊>The European Journal of Neuroscience >Oscillatory activity in the cortico‐basal ganglia‐thalamic neural circuits in Parkinson's disease
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Oscillatory activity in the cortico‐basal ganglia‐thalamic neural circuits in Parkinson's disease

机译：帕金森病皮里科基底神经节 - 丘陵神经电路的振荡活动

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Abstract Dopamine is an important neurotransmitter that maintains the balance within the basal ganglia between the direct pathway, which promotes movement, and the indirect pathway, which inhibits movement. Degeneration of dopaminergic neurons in the substantia nigra increases the influence of the indirect pathway, resulting in motor dysfunction in Parkinson's disease ( PD ). The direct and indirect pathways are composed of basal ganglia and thalamic nuclei, which are interconnected via independent parallel loop circuits with cortical areas and often referred to as cortico‐basal ganglia‐thalamic ( CBT ) neural circuits. CBT circuits have been useful in generating hypotheses to describe slowness in PD . Recent work has focused on aberrant neural oscillations within CBT circuits. Although beta (13–30?Hz) oscillations are a common feature of the CBT network, there is growing evidence that abnormally exaggerated beta oscillations, observed after dopamine loss in the CBT circuits, may contribute to motor symptoms of PD . Disruption of abnormal beta oscillations has been associated with the improvement of motor functions during pharmacological treatments, surgical lesions, and electrical stimulation. However, it is not clear how abnormal oscillations originate in the CBT motor network and resonate specifically in the beta band after the loss of dopamine. Most studies have addressed these questions by simultaneous recordings of oscillations in the motor cortex, basal ganglia nuclei, and motor regions of the thalamus in animal models of parkinsonism as well as in PD patients. This review further discusses previous and current studies of the changes in oscillatory activity at the level of CBT neural network in PD .
机译：摘要多巴胺是一种重要的神经递质，可在促进运动的直接途径和间接途径之间维持基底神经节的平衡。在Implia NIGRA中的多巴胺能神经元的退化增加了间接途径的影响，导致帕金森病（PD）的电动机功能障碍。直接和间接途径由基底神经节和丘脑组成，其通过与皮质区域的独立并行环路电路互连，并且通常被称为皮质基底神经节 - 丘脑（CBT）神经电路。 CBT电路在生成假设中是有用的，以描述PD中的慢速。最近的工作专注于CBT电路内的异常神经振荡。虽然Beta（13-30？Hz）振荡是CBT网络的共同特征，但越来越多的证据表明，在CBT电路中的多巴胺损失后观察到异常夸张的β振荡可能有助于PD的电机症状。异常β振荡的破坏与药理学治疗，手术病变和电刺激的改善有关。然而，目前尚不清楚振荡异常源于CBT电机网络，并在失去多巴胺后特别在β带中的共鸣。大多数研究通过同时录制了帕金森主义动物模型以及PD患者的马达皮质，基础神经节核和丘脑的运动区域的振荡来解决这些问题。本综述进一步讨论了PD中CBT神经网络水平的振荡活动变化的先前和目前研究。

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