当前位置: X-MOL 学术Acta Pharmacol. Sin. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Synaptic and cellular plasticity in Parkinson's disease.
Acta Pharmacologica Sinica ( IF 6.9 ) Pub Date : 2020-02-28 , DOI: 10.1038/s41401-020-0371-0
Hong-Yuan Chu 1, 2
Affiliation  

Parkinson's disease (PD) is a progressive neurodegenerative disease, which causes a tremendous socioeconomic burden. PD patients are suffering from debilitating motor and nonmotor symptoms. Cardinal motor symptoms of PD, including akinesia, bradykinesia, resting tremor, and rigidity, are caused by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. In addition, decreased amounts of dopamine (DA) level in the basal ganglia induces numerous adaptive changes at the cellular and synaptic levels in the basal ganglia circuits. These cellular and synaptic adaptations are believed to underlie the emergence and propagation of correlated, rhythmic pattern of activity throughout the interconnected cortico-basal ganglia-thalamocortical network. The widespread pathological pattern of brain activity is closely linked to the devastating motor symptoms of PD. Accumulating evidence suggests that both dopaminergic degeneration and the associated abnormal cellular and circuit activity in the basal ganglia drive the motor symptoms of PD. In this short review I summarize the recent advances in our understanding of synaptic and cellular alterations in two basal ganglia nuclei (i.e. the striatum and the subthalamic nucleus) following a complete loss of DA, and in our conceptual understanding of the cellular and circuit bases for the pathological pattern of brain activity in parkinsonian state.

中文翻译:

帕金森氏病中的突触和细胞可塑性。

帕金森氏病(PD)是一种进行性神经退行性疾病,会造成巨大的社会经济负担。PD患者患有使运动和非运动症状恶化的疾病。PD的主要运动症状包括运动障碍,运动迟缓,静息性震颤和僵硬,是由黑质致密部中的多巴胺能神经元变性引起的。另外,基底神经节中多巴胺(DA)水平的降低会引起基底神经节回路中细胞和突触水平的许多适应性变化。这些细胞和突触的适应被认为是整个相互联系的皮质-基底神经节-丘脑皮质网络中相关的节律性活动模式的出现和传播的基础。脑活动的广泛病理模式与PD毁灭性运动症状密切相关。越来越多的证据表明,多巴胺能变性以及基底神经节中相关的异常细胞和电路活动均会驱动PD的运动症状。在这篇简短的综述中,我总结了在完全丧失DA后我们对两个基底神经节核(即纹状体和丘脑下核)的突触和细胞改变的理解以及对我们的细胞和电路基础的概念理解方面的最新进展。帕金森病状态下脑活动的病理模式。
更新日期:2020-02-28
down
wechat
bug