A neuronal process of the error signal that drives saccade adaptation

驱动扫视适应的误差信号的神经元过程

• 批准号: 10213731
• 负责人: Yoshiko Kojima
• 金额: $ 44.4万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2013
• 资助国家: 美国
• 起止时间: 2013-08-01 至 2023-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10213731
• 关键词: Affect; Age; Aging; Agonist; Basal Ganglia; Behavioral; Biological Models; Brain; Cerebellar Cortex; Cerebellar vermis structure; Cerebellum; Characteristics; Clinical Research; Complex; Dissociation; Dysmetria; Fiber; Fingers; Funding; Goals; Grant; Hyperactivity; Inferior; Injections; Injury; Learning; Measures; Modeling; Monkeys; Motor; Movement; Muscimol; Nervous System Trauma; Neurons; Noise; Olives - dietary; Outcome; Output; Parkinson Disease; Pathway interactions; Patients; Process; Purkinje Cells; Recovery; Rehabilitation therapy; Role; Saccades; Shapes; Side; Signal Transduction; Source; Speed; Stroke; Structure; Substantia nigra structure; System; Testing; Theoretical model; Visual; dopaminergic neuron; experimental study; improved; insight; motor impairment; motor learning; neuromechanism; neurophysiology; oculomotor; relating to nervous system; repaired; response; superior colliculus Corpora quadrigemina

Project Summary/Abstract An impaired movement due to stroke, injury or aging recovers gradually. Can we speed up the recovery process to achieve the rehabilitation faster? To repair an inaccurate movement, the brain measures the error of the movement, namely the mismatch between the desired movement and the actual dysmetric movement, and changes the movement to minimize the error. This process is called motor adaptation. The speed of adaptation depends on its sensitivity to the error, i.e., the higher the error sensitivity, the faster the adaptation. Theoretical models and neurophysiological studies suggest that the complex spikes of Purkinje cells in the cerebellum encode the error. However, the neurons that deal with the error sensitivity are unknown. Knowing the neuronal mechanisms that control error sensitivity has important implications for setting strategies for the most efficient recovery strategy. In our last grant, we used saccade adaptation as a model system of motor adaptation. When we arranged that each saccade missed its target by a constant error, the adaptation speed decreased gradually during the adaptation session. This indicates that the sensitivity to the constant error decreased during the session. We found that the visual sensitivity of superior colliculus (SC) neurons decreased as the error sensitivity decreased. The visual activity of the SC has been suggested as a source of the complex spikes in the cerebellum, which encode the error of the movement. Therefore, the SC visual activity could provide an error sensitivity signal to the cerebellum. In this next grant period, we propose to examine how the visual activity of SC neurons is shaped to encode the error sensitivity. Many brain structures project to the SC, but one of the best candidates to shape SC activity is the Substantia Nigra pars reticulata (SNr) of the basal ganglia because it inhibits the SC directly. Moreover, because patients with Parkinson’s disease, which affects the basal ganglia, show a slower saccade adaptation, it seems likely that the basal ganglia affect the signal that controls the adaptation speed. To test this hypothesis, we will study the SNr with three complementary approaches. First, we will record SNr activity during saccade adaptation and determine whether any component of SNr discharge is related to error sensitivity. Second, we will determine the effect of SNr inactivation on saccade adaptation. We expect that inactivation will affect the adaptation speed. Third, we will determine the effect that SNr inactivation has on the activity of SC neurons. We expect that SNr inactivation will influence the visual activity of neurons in the rostral SC, which is related to the error sensitivity. We predict that the results of these three projects will reveal a previously unsuspected role for the basal ganglia in controlling the adaptation speed for cerebellar-dependent motor adaptation.

项目概要/摘要 由于中风、受伤或衰老而导致的运动受损会逐渐恢复。我们可以加快 恢复过程如何更快地实现康复？为了修复不准确的运动，大脑会测量 运动误差，即期望运动与实际运动失调之间的不匹配 运动，并改变运动以最小化误差。这个过程称为运动适应。这 适应的速度取决于其对误差的敏感度，即误差敏感度越高，适应的速度越快。 适应。理论模型和神经生理学研究表明，浦肯野病毒的复杂尖峰 小脑细胞对错误进行编码。然而，处理错误敏感性的神经元尚不清楚。 了解控制错误敏感性的神经机制对于制定策略具有重要意义 最有效的恢复策略。 在我们的上一次资助中，我们使用眼跳适应作为运动适应的模型系统。当我们 安排每次扫视都以恒定的误差错过目标，适应速度逐渐下降 在适应会议期间。这表明对恒定误差的敏感度在 会议。我们发现上丘（SC）神经元的视觉敏感性随着误差的增加而降低。 敏感性下降。 SC 的视觉活动被认为是复杂尖峰的来源 小脑，编码运动误差。因此，SC视觉活动可以提供 向小脑发出的错误敏感信号。 在下一个资助期内，我们建议研究 SC 神经元的视觉活动是如何形成的 对错误敏感度进行编码。许多大脑结构都投射到 SC，但塑造 SC 的最佳候选结构之一 SC 活性是基底神经节的黑质网状部 (SNr)，因为它直接抑制 SC。 此外，由于影响基底神经节的帕金森病患者的眼跳速度较慢 适应，基底神经节似乎可能影响控制适应速度的信号。 为了检验这个假设，我们将使用三种互补的方法来研究 SNr。首先，我们将 记录扫视适应期间的 SNr 活动并确定 SNr 放电的任何组成部分是否 与误差敏感度有关。其次，我们将确定 SNr 失活对眼跳适应的影响。我们 预计失活会影响适应速度。第三，我们将确定 SNr 的影响 失活对 SC 神经元的活性有影响。我们预计 SNr 失活会影响视觉活动 吻侧 SC 神经元的数量，这与错误敏感性有关。 我们预测这三个项目的结果将揭示基础细胞以前未曾怀疑的作用 神经节控制小脑依赖性运动适应的适应速度。