A role for NMDAR-dependent cerebellar plasticity in adaptive control of saccades in humans
A role for NMDAR-dependent cerebellar plasticity in adaptive control of saccades in humans
复制标题
DOI：
10.1016/j.brs.2017.05.001
复制
发表时间：
2017-07-01
影响因子：
7.7
通讯作者：
Ramat, S.
中科院分区：
文献类型：
--
作者：
Colnaghi, S.;Colagiorgio, P.;Ramat, S.
背景：眼跳脉冲幅度的适应是由小脑蚓背和顶状核介导的。平行纤维-珀金杰细胞突触的长期抑制为相应的学习过程提供了一种细胞机制。然而，这种可塑性的机制和位置仍然存在争议。目的：探讨小脑可塑性现象在自适应扫视控制中的作用。方法：观察后蚓连续θ波爆发刺激（cTBS）对扫视振幅适应和初始反应自发恢复的影响。为了进一步确定导致适应性损伤的突触可塑性底物，研究人员对受试者进行了n -甲基-o-天冬氨酸受体（NMDAR）拮抗剂美金刚的预处理。结果：cTBS改变了振幅适应，提示cTBS干扰了参与跳眼适应的小脑可塑性。当录音前给予美金刚时，cTBS不影响振幅适应和自发恢复。结论：cTBS的作用是nmdar依赖性的，可能涉及颗粒层和分子层特定突触连接的长时程增强或长时程抑制，有效参与小脑运动学习。(C) 2017爱思唯尔公司版权所有。
Background: Saccade pulse amplitude adaptation is mediated by the dorsal cerebellar vermis and fastigial nucleus. Long-term depression at the parallel fibre-Purkinjie cell synapses has been suggested to provide a cellular mechanism for the corresponding learning process. The mechanisms and sites of this plasticity, however, are still debated.Objective: To test the role of cerebellar plasticity phenomena on adaptive saccade control.Methods: We evaluated the effect of continuous theta burst stimulation (cTBS) over the posterior vermis on saccade amplitude adaptation and spontaneous recovery of the initial response. To further identify the substrate of synaptic plasticity responsible for the observed adaptation impairment, subjects were pre-treated with memantine, an N-methyl-o-aspartate receptor (NMDAR) antagonist.Results: Amplitude adaptation was altered by cTBS, suggesting that cTBS interferes with cerebellar plasticity involved in saccade adaptation. Amplitude adaptation and spontaneous recovery were not affected by cTBS when recordings were preceded by memantine administration.Conclusion: The effects of cTBS are NMDAR-dependent and are likely to involve long-term potentiation or long-term depression at specific synaptic connections of the granular and molecular layer, which could effectively take part in cerebellar motor learning. (C) 2017 Elsevier Inc. All rights reserved.