Tachibana Yoshihisa, Kita Hitoshi, Chiken Satomi, Takada Masahiko, Nambu Atsushi
Division of System Neurophysiology, National Institute for Physiological Sciences, The Graduate University for Advanced Studies, Myodaiji, Okazaki 444-8585, Japan.
Eur J Neurosci. 2008 Jan;27(1):238-53. doi: 10.1111/j.1460-9568.2007.05990.x. Epub 2007 Dec 17.
The internal segment of the globus pallidus (GPi) receives motor-related cortical signals mainly through the striatum, the external segment of the globus pallidus (GPe) and the subthalamic nucleus (STN). The GPi sends its outputs outside the basal ganglia and plays a key role in motor control. Extracellular unit recordings were performed in awake monkeys to explore how glutamatergic STN inputs and GABAergic striatal and GPe inputs control spontaneous activity and how these inputs contribute to motor cortex stimulation-induced responses of GPi neurons. The typical responses of GPi neurons to cortical stimulation consisted of an early excitation, an inhibition and a late excitation. Local applications of the NMDA receptor antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid and/or the AMPA/kainate receptor antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[f]quinoxaline-7-sulphonamide in the vicinity of recorded GPi neurons reduced the firing rate, and abolished or attenuated both early and late excitations following cortical stimulation. Local application of the GABA(A) receptor antagonist gabazine increased the firing rate, induced oscillatory firings and diminished the cortically induced inhibition. Muscimol or gabazine injection into the STN or GPe also altered the firing rate, and attenuated the late excitation of GPi neurons. The gabazine injection into the STN occasionally induced dyskinesia with significantly decreased GPi activity. These data suggest that the early and late excitations are glutamatergic and induced by the cortico-STN-GPi and cortico-striato-GPe-STN-GPi pathways, respectively. The inhibition is GABAergic and induced by the cortico-striato-GPi pathway. In addition, these inputs are the main factors governing the spontaneous activity of GPi neurons.
苍白球内侧段（GPi）主要通过纹状体、苍白球外侧段（GPe）和底丘脑核（STN）接收与运动相关的皮质信号。GPi将其输出信号发送到基底神经节之外，并在运动控制中发挥关键作用。在清醒的猴子身上进行了细胞外单位记录，以探究谷氨酸能的STN输入以及GABA能的纹状体和GPe输入如何控制自发活动，以及这些输入如何促成运动皮层刺激诱发的GPi神经元反应。GPi神经元对皮层刺激的典型反应包括早期兴奋、抑制和晚期兴奋。在记录的GPi神经元附近局部应用NMDA受体拮抗剂3-(2-羧基哌嗪-4-基)-丙基-1-膦酸和/或AMPA/海人藻酸受体拮抗剂1,2,3,4-四氢-6-硝基-2,3-二氧代-苯并[f]喹喔啉-7-磺酰胺，可降低放电频率，并消除或减弱皮层刺激后的早期和晚期兴奋。局部应用GABA(A)受体拮抗剂荷包牡丹碱可提高放电频率，诱发振荡性放电，并减弱皮层诱导的抑制。向STN或GPe注射蝇蕈醇或荷包牡丹碱也会改变放电频率，并减弱GPi神经元的晚期兴奋。向STN注射荷包牡丹碱偶尔会诱发运动障碍，同时GPi活动显著降低。这些数据表明，早期和晚期兴奋是谷氨酸能的，分别由皮质-STN-GPi和皮质-纹状体-GPe-STN-GPi通路诱发。抑制是GABA能的，由皮质-纹状体-GPi通路诱发。此外，这些输入是控制GPi神经元自发活动的主要因素。
