The dynamical properties of cortico-basal ganglia (CBG) circuits are dramatically altered following the loss of dopamine in Parkinson’s disease (PD). The neural circuit dysfunctions associated with PD include spike-rate alteration concomitant with excessive oscillatory spike-synchronization in the beta frequency range (12–30 Hz). Which neuronal circuits orchestrate and propagate these abnormal neural dynamics in CBG remains unknown. In this work, we combine in vivo electrophysiological recordings with advanced optogenetic manipulations in normal and 6-OHDA rats to shed light on the mechanistic principle underlying circuit dysfunction in PD. Our results show that abnormal neural dynamics present in a rat model of PD do not rely on cortical or subthalamic nucleus activity but critically dependent on globus pallidus (GP) integrity. Our findings highlight the pivotal role played by the GP which operates as a hub nucleus capable of orchestrating firing rate and synchronization changes across CBG circuits both in normal and pathological conditions.

帕金森病（PD）中多巴胺的流失后，皮质基底神经节（CBG）回路的动力学特性发生了巨大变化。与PD相关的神经回路功能障碍包括在β频率范围（12–30 Hz）中伴随着过多的振荡尖峰同步的尖峰速率改变。哪些神经回路协调和传播这些异常的神经动力学在CBG中仍然是未知的。在这项工作中，我们将体内电生理学记录与正常和6-OHDA大鼠中的先进光遗传学操作相结合，以阐明PD中电路功能障碍的机制原理。我们的研究结果表明，PD大鼠模型中存在的异常神经动力学并不依赖于皮质或丘脑底核活性，而是严重依赖于苍白球（GP）完整性。