The basal ganglia are an intricately connected assembly of subcortical nuclei, forming the core of an adaptive network connecting cortical and thalamic circuits. For nearly three decades, researchers and medical practitioners have conceptualized how the basal ganglia circuit works, and how its pathology underlies motor disorders such as Parkinson's and Huntington's diseases, using what is often referred to as the "box-and-arrow model": a circuit diagram showing the broad strokes of basal ganglia connectivity and the pathological increases and decreases in the weights of specific connections that occur in disease. While this model still has great utility and has led to groundbreaking strategies to treat motor disorders, our evolving knowledge of basal ganglia function has made it clear that this classic model has several shortcomings that severely limit its predictive and descriptive abilities. In this review, we will focus on the striatum, the main input nucleus of the basal ganglia. We describe recent advances in our understanding of the rich microcircuitry and plastic capabilities of the striatum, factors not captured by the original box-and-arrow model, and provide examples of how such advances inform our current understanding of the circuit pathologies underlying motor disorders.

中文翻译：

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跳出框框思考（和箭头）：运动障碍中纹状体功能障碍的当前主题。

基底神经节是皮层下核的复杂连接的组件，形成了连接皮层和丘脑回路的自适应网络的核心。近三十年来，研究人员和医学从业人员使用通常被称为“框箭模型”的概念，对基底神经节回路如何工作以及其病理学是诸如帕金森氏病和亨廷顿氏病等运动障碍的基础概念进行了研究：电路图显示了基底神经节连接的广泛冲程以及疾病中特定连接的权重在病理上的增加和减少。尽管此模型仍然具有很大的实用性，并已导致开创性的治疗运动障碍的策略，我们对基底神经节功能的不断发展的知识已经清楚地表明，这种经典模型存在一些缺点，严重限制了其预测和描述能力。在本文中，我们将重点关注纹状体，即基底神经节的主要输入核。我们描述了对纹状体丰富的微电路和可塑性的理解方面的最新进展，以及原始框和箭头模型未捕获的因素，并提供了这些进展如何举例说明我们当前对运动障碍潜在电路病理的了解的示例。