Basal Ganglia Pathophysiology Unit, Department of Experimental Medical Science, Lund University, BMC A13, 221 84, Lund, Sweden.
The Group for Integrative Neurophysiology and Neurotechnology, Department of Experimental Medical Science, Lund University, Lund, Sweden.
Neurotherapeutics. 2023 Jan;20(1):304-324. doi: 10.1007/s13311-022-01309-5. Epub 2022 Nov 7.
L-DOPA-induced dyskinesia (LID) in Parkinson's disease has been linked to oscillatory neuronal activities in the cortico-basal ganglia network. We set out to examine the pattern of cortico-basal ganglia oscillations induced by selective agonists of D1 and D2 receptors in a rat model of LID. Local field potentials were recorded in freely moving rats using large-scale electrodes targeting three motor cortical regions, dorsomedial and dorsolateral striatum, external globus pallidus, and substantial nigra pars reticulata. Abnormal involuntary movements were elicited by the D1 agonist SKF82958 or the D2 agonist sumanirole, while overall motor activity was quantified using video analysis (DeepLabCut). Both SKF82958 and sumanirole induced dyskinesia, although with significant differences in temporal course, overall severity, and body distribution. The D1 agonist induced prominent narrowband oscillations in the high gamma range (70-110 Hz) in all recorded structures except for the nigra reticulata. Additionally, the D1 agonist induced strong functional connectivity between the recorded structures and the phase analysis revealed that the primary motor cortex (forelimb area) was leading a supplementary motor area and striatum. Following treatment with the D2 agonist, narrowband gamma oscillations were detected only in forelimb motor cortex and dorsolateral striatum, while prominent oscillations in the theta band occurred in the globus pallidus and nigra reticulata. Our results reveal that the dyskinetic effects of D1 and D2 receptor agonists are associated with distinct patterns of cortico-basal ganglia oscillations, suggesting a recruitment of partially distinct networks.
左旋多巴诱导的帕金森病运动障碍(LID)与皮质基底节网络中的振荡神经元活动有关。我们旨在检查 D1 和 D2 受体选择性激动剂在 LID 大鼠模型中诱导的皮质基底节振荡模式。使用针对三个运动皮质区域、背内侧和背外侧纹状体、外苍白球和黑质网状部的大规模电极,在自由移动的大鼠中记录局部场电位。异常不自主运动由 D1 激动剂 SKF82958 或 D2 激动剂 sumanirole 诱发,而总体运动活动则使用视频分析(DeepLabCut)进行量化。SKF82958 和 sumanirole 均诱发运动障碍,尽管在时间过程、总体严重程度和身体分布方面存在显著差异。D1 激动剂在除黑质网状部以外的所有记录结构中诱导出明显的高频带(70-110 Hz)窄带振荡。此外,D1 激动剂诱导了记录结构之间的强功能连接,相位分析表明,初级运动皮层(前肢区)领先于辅助运动区和纹状体。在用 D2 激动剂治疗后,仅在前肢运动皮层和背外侧纹状体中检测到窄带伽马振荡,而在苍白球和黑质网状部中则出现明显的 theta 带振荡。我们的结果表明,D1 和 D2 受体激动剂的运动障碍效应与皮质基底节振荡的不同模式相关,表明部分不同的网络被招募。