Hirsch E C, Périer C, Orieux G, François C, Féger J, Yelnik J, Vila M, Levy R, Tolosa E S, Marin C, Trinidad Herrero M, Obeso J A, Agid Y
INSERM U289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, Paris, France.
Trends Neurosci. 2000 Oct;23(10 Suppl):S78-85. doi: 10.1016/s1471-1931(00)00021-5.
In the past, functional changes in the circuitry of the basal ganglia that occur in Parkinson's disease were primarily analyzed with electrophysiological and 2-deoxyglucose measurements. The increased activity of the subthalamic nucleus (STN) observed has been attributed to a reduction in inhibition mediated by the external segment of the globus pallidus (GPe), secondary to the loss of dopaminergic-neuron influence on D2-receptor-bearing striato-pallidal neurons. More recently, in situ hybridization studies of cytochrome oxidase subunit I have confirmed the overactivity of the STN in the parkinsonian state. In addition, this technique has provided evidence that the change in STN activity is owing not only to decreased inhibition from the GPe but to hyperactivity of excitatory inputs from the parafascicular nucleus of the thalamus and the pedunculopontine nucleus in the brainstem.
过去，帕金森病中基底神经节神经回路的功能变化主要通过电生理和2-脱氧葡萄糖测量来分析。观察到的丘脑底核（STN）活动增加归因于苍白球外侧部（GPe）介导的抑制作用减弱，这是由于多巴胺能神经元对表达D2受体的纹状体苍白球神经元的影响丧失所致。最近，细胞色素氧化酶亚基I的原位杂交研究证实了帕金森病状态下STN的过度活跃。此外，该技术还提供了证据表明，STN活动的变化不仅是由于来自GPe的抑制作用减弱，还由于来自丘脑束旁核和脑干脚桥核的兴奋性输入过度活跃。
