CEREBELLAR NUCLEI IN EYE MOVEMENT CONTROL AND ADAPTATION

扫视、平稳追逐和收敛需要极其准确，才能提供清晰的视野。小脑的损伤严重损害了所有这三种自主眼球运动，并在眼球运动反复不准确时丧失了适应眼球运动的能力。我们不知道小脑对自主眼球运动的贡献，使它们在短期内变得准确，并在长期内适应它们。这项拟议的研究将研究小脑的一个关键部分--CFN对自主眼动的贡献。CFN(尾侧顶核)将信号从小脑发送到移动眼睛的回路。这些信号通过在每个动作中添加适当的水平分量，使扫视和追逐变得准确。我们提出，CFN可以像在短期内一样，通过增加必要的水平分量，在长期内使自愿眼球运动变得准确。我们将通过在行为正常的猴子身上使用单细胞记录和临时CFN损伤来测试这一提议，以确定CFN是否增加了适应扫视和追逐所需的水平分量。以前的工作没有描述小脑任何部分在适应任何自愿运动中的具体作用，尽管人们普遍认为适应是小脑的一种功能。我们还将使用记录和暂时性损害来观察CFN是否提供了适当的水平分量，以导致在眼跳过程中发生的高速收敛。同样，以前的工作没有描述这种跳动的神经机制，尽管这些动作是我们最常见的动作之一。CFN具有适当的解剖联系和反应特性，可以发挥重要作用。无论结果如何，这项拟议的研究将提供第一批关于适应自主眼球运动和眼跳收敛的神经机制的数据。这些数据肯定会提高我们对这些功能的理解，并帮助我们了解人类小脑患者的适应和收敛缺陷。我们的结果可能具体地表明，CFN提供了适当的水平驱动力来支持适应以及扫视、追逐和扫视-收敛。因此，CFN对移动的长期和短期影响只是相同产出的两个后果。这两个明显不同的CFN功能的统一观点将为理解其他小脑输出在控制和适应其他自愿运动中的作用提供第一个明确的模型。

Saccades, smooth pursuit, and vergence need to be extremely accurate to provide clear vision. Lesions of the cerebellum severely impair all three of these voluntary eye movements and abolish the ability to adapt eye movements when they are repeatedly inaccurate. We do not know what the cerebellum contributes to voluntary eye movements to make them accurate in the short-term and to adapt them in the long-term. The proposed research will study the contribution of one critical part of the cerebellum, the CFN, to voluntary eye movements. The CFN (caudal fastigial nucleus) send signals from the cerebellum to circuits that move the eyes. These signals make saccades and pursuit accurate by adding the proper horizontal component to each movement. We proposed that the CFN makes voluntary eye movements accurate in the long-term like it does in the short-term, i.e., by adding the necessary horizontal component. We will test this proposal by using single cell recording and temporary CFN lesions in behaving monkeys to determine if the CFN adds the horizontal component necessary to adapt saccades and pursuit. No previous work describes the specific role of any part of the cerebellum in adapting any voluntary movement, despite the act that adaptation is a function widely ascribed to the cerebellum. We will also use recording and temporary lesions to see if the CFN provides the appropriate horizontal component to cause the high speed vergence that occurs during saccades. Again, no previous work describes the neural mechanism of this saccadic-vergence though these movements are among the most common we make. The CFN has the appropriate anatomical connections and response properties to play a major role. Whatever its outcome, the proposed research will provide the first data on the neural mechanisms for adapting voluntary eye movements and for saccadic vergence. This data will certainly improve our understanding Of these functions and help us understand the adaptation and vergence deficits of human cerebellar patients. Our results may show specifically that the CFN provides the appropriate horizontal drive to support adaptation as well as saccades, pursuit, and saccadic-vergence. Thus, the CFN's long- and short-term effects on movement are simply two consequences of the same output. This unified view of two apparently different CFN functions would provide the first explicit model for understanding the role of other cerebellar output in controlling and adapting other voluntary movements.