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: 9325519
• 负责人: Yoshiko Kojima
• 金额: $ 44.5万
• 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/9325519
• 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; Impairment; 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; Research; Role; Route; Saccades; Scanning; Sensory; Side; Signal Pathway; Signal Transduction; Stimulus; Stroke; Testing; Time; Training; Visual; Wit; electrical microstimulation; improved; insight; microstimulation; motor deficit; motor recovery; 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）：电动机适应是在与中风，伤害或衰老引起的与神经损害相关的运动缺陷恢复功能的重要因素。这种电动机回收或适应性是由错误信号指示的 所需运动与实际运动之间的不匹配的大脑。但是，尚不了解处理特定误差信号的大脑电路。我的研究的长期目标是确定处理误差信号以优化感觉运动行为的神经机制。了解这些机制及其基础的电路将有助于为运动缺陷设计康复疗法。 我们已经通过使用猴子的眼球运动来实现我们的目标，该动作提供了理想的模型，因为扫视精确，只使用少数肌肉，相关的脑干神经回路已得到充分记录，并且可以通过良好的行为范式通过良好的行为进行运动。到目前为止，我们知道动眼刺（OMV）中的复杂尖峰发射编码运动误差，并且OMV是适应靶向扫视所必需的。 OMV中的复杂尖峰起源于下橄榄的一部分，该橄榄会从上丘（SC）接收投影。以前，我们已经表明，SC的电气微刺激与模拟视觉误差信号的时机诱导了扫视适应性。因此，SC似乎是误差信号途径的重要组成部分。 在这项研究中，我们提出了三个项目，以测试SC在编码扫视适应性的错误信号中的参与。第一个项目旨在确定是否需要SC来适应靶向扫视。我们将在此期间预测猴子在受到行为适应范式时无法适应其扫视。第二个项目旨在识别SC视觉活动中的相关性与驱动适应性的视觉误差信号的相关性。我们将寻找SC视觉活动WIT误差大小的相关性（小于大型误差的适应性比大型误差更好），并且具有适应率，随着适应性的进行而降低。第三个项目将确定SC是否也用于适应其他类型的扫视，包括内存引导，延迟，扫描和Express。我们将在其中一种不同类型的一种以模拟误差后向SC进行电气刺激 信号并确定有关瞄准扫视是否会导致适应性的人造错误。我确实如此，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确立SC在扫视适应中的先前没有引起的角色。