Role of ionotropic glutamatergic and GABAergic inputs on the firing activity of neurons in the external pallidum in awake monkeys
Role of ionotropic glutamatergic and GABAergic inputs on the firing activity of neurons in the external pallidum in awake monkeys
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DOI：
10.1152/jn.00346.2004
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发表时间：
2004-11-01
影响因子：
2.5
通讯作者：
Takada, M
中科院分区：
文献类型：
--
作者：
Kita, H;Nambu, A;Takada, M
清醒动物苍白球外段（GPe）的神经元保持高水平的放电活动。这种活动的水平和模式随着基底神经节疾病的发展而改变，包括帕金森综合征和偏侧投掷症。GPe投射到基底神经节的大部分核团。因此，探索控制放电活动的机制对于理解正常和病理条件下基底神经节的功能至关重要。为了探索离子型谷氨酸能和GABA能输入GPe的作用，在清醒的猴子中进行了结合局部注射受体拮抗剂的单位记录。观察局部应用α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）/红藻氨酸拮抗剂1，2，3，4-四氢-6-硝基-2，3-二氧代-苯并[f]喹喔啉-7-磺酰胺、N-甲基-D-天冬氨酸（NMDA）拮抗剂3-甲基-D-天冬氨酸（NMDA）拮抗剂的作用。（2-羧基哌嗪-4-基）-丙基-1-膦酸和GABA（A）拮抗剂gabazine以及蝇蕈醇阻断丘脑底核对自发放电率的影响，GPe神经元的自发放电模式和皮层刺激诱导的反应表明：持续的谷氨酸能和GABA能输入控制GPe神经元的自发放电水平，AMPA/红藻氨酸和NMDA受体都被谷氨酸能输入激活，有些GPe神经元接受来自丘脑底核以外区域的谷氨酸能输入;没有GPe神经元在谷氨酸和GABA拮抗剂的联合应用后变得沉默，这表明GPe神经元具有内在特性或非离子亲性谷氨酸能紧张性输入，其维持GPe神经元中的快速振荡放电或快速和缓慢振荡放电的组合。
The neurons in the external segment of the pallidum (GPe) in awake animals maintain a high level of firing activity. The level and pattern of the activity change with the development of basal ganglia disorders including parkinsonism and hemiballism. The GPe projects to most of the nuclei in the basal ganglia. Thus exploring the mechanisms controlling the firing activity is essential for understanding basal ganglia function in normal and pathological conditions. To explore the role of ionotropic glutamatergic and GABAergic inputs to the GPe, unit recordings combined with local injections of receptor antagonists were performed in awake monkeys. Observations on the effects of local application of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate antagonist 1,2,3,4-tetrahydro-6-nitro-2, 3-dioxo-benzo[f]quinoxaline-7-sulfonamide, the N-methyl-D-aspartic acid (NMDA) antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and the GABA(A) antagonist gabazine as well as the effects of muscimol blockade of the subthalamic nucleus on the spontaneous firing rate, firing patterns, and cortical stimulation induced responses in the GPe suggested the following: sustained glutamatergic and GABAergic inputs control the level of the spontaneous firing of GPe neurons; both AMPA/kainate and NMDA receptors are activated by glutamatergic inputs; some GPe neurons receive glutamatergic inputs originating from areas other than the subthalamic nucleus; no GPe neurons became silent after a combined application of glutamate and GABA antagonists, suggesting that GPe neurons have intrinsic properties or nonionotropic glutamatergic tonic inputs that sustain a fast oscillatory firing or a combination of a fast and a slow oscillatory firing in GPe neurons.