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: 8704942
• 负责人: Yoshiko Kojima
• 金额: $ 43.61万
• 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 2018-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8704942
• 关键词: Affect; Aging; Agonist; Behavior; Behavioral; Behavioral Paradigm; Brain; Brain Stem; Cerebellar cortex structure; Cerebellar vermis structure; Characteristics; Code; Complex; Contralateral; Delayed Memory; Error Sources; Exhibits; Fiber; Goals; Inferior; Injection of therapeutic agent; Injury; Ipsilateral; Maintenance; Memory; Modeling; Monkeys; Motor; Movement; Muscimol; Muscle; Neurons; Olives - dietary; Outcome; Pathway interactions; Play; Process; Property; Recovery; Recovery of Function; Rehabilitation therapy; Relative (related person); Research; Role; Route; Saccades; Scanning; Sensory; Side; Signal Pathway; Signal Transduction; Stimulus; Stroke; Testing; Time; Training; Visual; Wit; improved; insight; motor deficit; neural circuit; neuromechanism; oculomotor; preference; public health relevance; relating to nervous system; superior colliculus Corpora quadrigemina; vector

DESCRIPTION (provided by applicant): Motor adaptation is an important factor in the recovery of function following motor deficits associated with neural damage due to stroke, injury or aging. Such motor recovery or adaptation, is instructed by an error signal that is calculated by the brain from the mismatch between the desired movement and the actual movement produced. However, the brain circuits that process specific error signal(s) are not understood. The long-term goal of my research is to identify the neural mechanisms that process error signals to optimize sensory-motor behavior. Understanding these mechanisms and the circuitry underlying them will assist in devising rehabilitation therapies for motor deficits. We have approached our goal by using monkey saccadic eye movements, which provide an ideal model because saccades are precise, use only a few muscles, the associated brainstem neural circuit has been well documented and they can be made to undergo motor adaptation by means of well-established behavioral paradigms. Thus far, we know that complex spike firing in the oculomotor vermis (OMV) encodes motor error and that the OMV is required for adaptation of targeting saccades. Complex spikes in the OMV originate in a part of the inferior olive that receives a projection from the superior colliculus (SC). Previously, we have shown that electrical micro-stimulation of the SC, timed to mimic visual error signals, induces saccade adaptation. Thus, the SC appears to be an important part of the error signal pathway. In this study, we propose three projects to test the involvement of the SC in coding an error signal for saccade adaptation. The first project is directed at determining whether the SC is required for adaptation of targeting saccades. We will inactivate the SC reversibly during which time we predict that the monkey will be unable to adapt its saccades when subjected to a behavioral adaptation paradigm. The second project is directed at identifying correlates in SC visual activity with the visual error signal that drives adaptation. We will look for correlations of SC visual activity wit error size (small errors drive adaptation better than large ones) and with adaptation rate, which decreases as adaptation progresses. The third project will determine whether the SC is also used for adaptation of other types of saccade, including memory-guided, delayed, scanning and express. We will electrically stimulate the SC after one of these different types to mimic an error signal and determine whether, as for targeting saccades, this artificial error causes adaptation. I it does, we will test whether the adaptation transfers to the other types. We anticipate that together the results of these three projects will help establish a previously unsuspected role for the SC in saccade adaptation.

描述(由申请人提供)：运动适应是中风、损伤或衰老导致的神经损伤导致的运动缺陷后恢复功能的重要因素。这种马达恢复或适应由误差信号指示，该误差信号由下式计算 大脑由期望的运动和实际的运动之间的不匹配产生。然而，处理特定误差信号的大脑回路(S)还不清楚。我研究的长期目标是确定处理错误信号以优化感觉-运动行为的神经机制。了解这些机制及其背后的电路将有助于设计运动障碍的康复疗法。我们已经通过使用猴子的眼跳运动来接近我们的目标，这提供了一个理想的模型，因为眼跳是精确的，只使用几块肌肉，相关的脑干神经回路已经被很好地记录下来，并且可以通过建立良好的行为模式来使它们经历运动适应。到目前为止，我们知道在动眼蠕虫(oculomomtor vermis，OMV)中复杂的棘波放电编码运动错误，并且OMV是适应靶向扫视所必需的。OMV中复杂的棘波起源于下橄榄接受上丘投射的部分。以前，我们已经证明，对SC的微刺激，定时模拟视觉错误信号，诱导眼跳适应。因此，SC似乎是错误信号通路的重要组成部分。在这项研究中，我们提出了三个项目来测试SC在编码错误信号以进行眼跳适应时的参与程度。第一个项目旨在确定是否需要SC来适应靶向扫视。我们将可逆地使SC失活，在此期间，我们预测猴子在受到行为适应范例的影响时，将无法适应其眼跳。第二个项目旨在确定SC视觉活动与驱动适应的视觉错误信号之间的相关性。我们将寻找SC视觉活动与错误大小(小错误比大错误更好地驱动适应)和适应率的相关性，后者随着适应的进展而下降。第三个项目将确定SC是否也用于适应其他类型的扫视，包括记忆引导、延迟、扫描和快速扫视。我们将在这些不同类型中的一种之后电刺激SC以模拟错误 发信号并确定对于目标扫视，该人为错误是否导致适应。如果是这样的话，我们将测试适应是否转移到其他类型。我们预计，这三个项目的结果将有助于为SC在眼跳适应方面建立一个以前未被怀疑的角色。