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基底节运动障碍的特异性丧失。

Loss of specificity in Basal Ganglia related movement disorders.

机构信息

The Leslie and Susan Gonda (Goldschmied) Multidisciplinary Brain Research Center, Bar-Ilan University Ramat-Gan, Israel.

出版信息

Front Syst Neurosci. 2011 Jun 3;5:38. doi: 10.3389/fnsys.2011.00038. eCollection 2011.

DOI:10.3389/fnsys.2011.00038
PMID:21687797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3108383/
Abstract

The basal ganglia (BG) are a group of interconnected nuclei which play a pivotal part in limbic, associative, and motor functions. This role is mirrored by the wide range of motor and behavioral abnormalities directly resulting from dysfunction of the BG. Studies of normal behavior have found that BG neurons tend to phasically modulate their activity in relation to different behavioral events. In the normal BG, this modulation is highly specific, with each neuron related only to a small subset of behavioral events depending on specific combinations of movement parameters and context. In many pathological conditions involving BG dysfunction and motor abnormalities, this neuronal specificity is lost. Loss of specificity (LOS) manifests in neuronal activity related to a larger spectrum of events and consequently a large overlap of movement-related activation patterns between different neurons. We review the existing evidence for LOS in BG-related movement disorders, the possible neural mechanisms underlying LOS, its effects on frequently used measures of neuronal activity and its relation to theoretical models of the BG. The prevalence of LOS in a many BG-related disorders suggests that neuronal specificity may represent a key feature of normal information processing in the BG system. Thus, the concept of neuronal specificity may underlie a unifying conceptual framework for the BG role in normal and abnormal motor control.

摘要

基底神经节(BG)是一组相互连接的核团,在边缘、联想和运动功能中起着关键作用。这种作用反映在由 BG 功能障碍直接导致的广泛的运动和行为异常中。对正常行为的研究发现,BG 神经元的活动往往与不同的行为事件相关地呈现相位调制。在正常的 BG 中,这种调制具有高度的特异性,每个神经元仅与一小部分行为事件相关,具体取决于运动参数和上下文的特定组合。在涉及 BG 功能障碍和运动异常的许多病理情况下,这种神经元特异性会丢失。特异性丧失(LOS)表现为与更大范围的事件相关的神经元活动,因此不同神经元之间的运动相关激活模式有很大的重叠。我们回顾了与 BG 相关运动障碍中的 LOS 存在的证据、LOS 潜在的神经机制、其对常用神经元活动测量的影响以及与 BG 理论模型的关系。在许多与 BG 相关的疾病中 LOS 的普遍性表明,神经元特异性可能代表了 BG 系统中正常信息处理的关键特征。因此,神经元特异性的概念可能是 BG 在正常和异常运动控制中的作用的统一概念框架的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/16bc979bf703/fnsys-05-00038-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/4052b1a32af7/fnsys-05-00038-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/42973d6f0575/fnsys-05-00038-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/3531ff9ab810/fnsys-05-00038-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/24e1e2873a06/fnsys-05-00038-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/16bc979bf703/fnsys-05-00038-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/4052b1a32af7/fnsys-05-00038-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/42973d6f0575/fnsys-05-00038-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/3531ff9ab810/fnsys-05-00038-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/24e1e2873a06/fnsys-05-00038-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad57/3108383/16bc979bf703/fnsys-05-00038-g005.jpg

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