丘脑底核神经元的丢失对帕金森病有保护作用吗？
Is the loss of thalamostriatal neurons protective in parkinsonism?
机构信息
Program in Neuroscience and Department of Psychiatry, Vanderbilt University Medical Center, Nashville, TN 37212, USA.
出版信息
Parkinsonism Relat Disord. 2009 Dec;15 Suppl 3(Suppl 3):S162-6. doi: 10.1016/S1353-8020(09)70806-5.
Abstract
Neuronal loss in Parkinson's disease (PD) is more widespread than originally thought. Among the extrastriatal sites in which significant loss of neurons has been reported is the centremedian-parafascicular (CM-PF) complex of the thalamus, which provides one of the three major afferent sources to the striatum. The functional significance of CM-PF loss in PD is unclear. Interestingly, several recent small trials have suggested that deep brain stimulation of the CM-PF improves motor function in PD. We discuss the possible transsynaptic determination of CM-PF loss secondary to nigrostriatal dopamine degeneration, and suggest that expression of the glycoprotein cerebellin1 (Cbln1) in CM-PF neurons may play an important role in striatal synaptic remodeling in parkinsonism.
摘要
帕金森病（PD）中的神经元丧失比最初认为的更为广泛。在报道有明显神经元丧失的纹状体以外的部位中，有丘脑的中央中缝核-旁正中（CM-PF）复合体，它为纹状体提供了三个主要传入源之一。PD 中 CM-PF 丧失的功能意义尚不清楚。有趣的是，最近的几项小型试验表明，CM-PF 的深部脑刺激可改善 PD 的运动功能。我们讨论了 CM-PF 丧失继发于黑质纹状体多巴胺变性的可能的突触传递性决定因素，并提出 CM-PF 神经元中糖蛋白小脑蛋白 1（Cbln1）的表达可能在帕金森病中的纹状体突触重塑中发挥重要作用。
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