Motor cortical control of internal pallidal activity through glutamatergic and GABAergic inputs in awake monkeys
Motor cortical control of internal pallidal activity through glutamatergic and GABAergic inputs in awake monkeys
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DOI：
10.1111/j.1460-9568.2007.05990.x
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发表时间：
2008-01-01
影响因子：
3.4
通讯作者：
Nambu, Atsushi
中科院分区：
文献类型：
--
作者：
Tachibana, Yoshihisa;Kita, Hitoshi;Nambu, Atsushi
苍白球内段（GPi）主要通过纹状体、苍白球外段（GPe）和丘脑底核（STN）接收运动相关的皮质信号。 GPi 将其输出发送到基底神经节之外，并在运动控制中发挥关键作用。在清醒的猴子中进行细胞外单位记录，以探索谷氨酸能 STN 输入和 GABA 能纹状体和 GPe 输入如何控制自发活动，以及这些输入如何促进运动皮层刺激诱导的 GPi 神经元反应。 GPi 神经元对皮质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/红藻氨酸受体拮抗剂 1,2,3,4-四氢-6-硝基-2,3-二氧代-苯并[f]喹喔啉-7-磺酰胺降低了放电率，并消除或减弱了皮层刺激后的早期和晚期兴奋。局部应用 GABA(A) 受体拮抗剂加巴嗪可增加放电频率，诱导振荡放电并减少皮质诱导的抑制。将蕈醇或加巴嗪注射到 STN 或 GPe 中也改变了放电速率，并减弱了 GPi 神经元的晚期兴奋。 STN 注射加巴嗪偶尔会引起运动障碍，并显着降低 GPi 活性。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 途径诱导。这种抑制是 GABA 能的，由皮质-纹状体-GPi 途径诱导。此外，这些输入是控制 GPi 神经元自发活动的主要因素。
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.