Neural control of coordinated eye movements

协调眼球运动的神经控制

基本信息

批准号：
10670910
负责人：
Julie Quinet
金额：
$ 37.13万
依托单位：
UNIVERSITY OF ALABAMA AT BIRMINGHAM
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-09-01 至 2026-07-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10670910
关键词：
3-Dimensional Amblyopia Anatomy Animals Area Brain region Cell Nucleus Cells Cerebellar Nuclei Cerebellum Code Complex Contralateral Convergence Insufficiency Data Electrophysiology (science)Elements Environment Esotropia Eye Eye Movements Functional disorder Generations Goals Impairment Individual Injections Lateral Maintenance Medial Modeling Motor Activity Motor Neurons Movement Muscimol Neural Interconnection Neurons Nucleus fastigii Oculomotor nucleus Pathway interactions Play Population Positioning Attribute Primates Production Reticular Formation Role Route Saccades Signal Transduction Strabismus Techniques Testing Time Visual abducens nucleus cell type disability electrical microstimulation experimental study gaze insight interest monocular neural neural circuit neural model neurophysiology neuroregulation novel oculomotor pharmacologic response sample fixation targeted imaging

项目摘要

Project Summary / Abstract We look between targets located in the 3D visual environment by making disjunctive saccades that bring the target image onto both foveae. Each gaze shift is followed by a fixation period for visual analysis during which the new vergence level must be maintained. Most studies have focused on the circuitry controlling conjugate saccades, whereas the neural control of disjunctive saccades and vergence eye movements has received less study. Several models suggest that abducens motoneurons send a monocular command carrying information to each eye to control disjunctive saccades. Other models have proposed the existence of saccade-vergence burst neurons (SVBNs) that project to medial rectus motoneurons and are active only during disjunctive saccades. We have identified this novel cell type, which only discharge during disjunctive saccades, in the central mesencephalic reticular formation (cMRF) lateral to the oculomotor nucleus (OMN). Electrical microstimulation in this region of the cMRF elicits disjunctive saccades, whereas inactivation impairs vergence gaze holding. Recent anatomical findings have demonstrated that premotor neurons related to the near response are located in the cMRF, and that they project to the supraoculomotor area (SOA) and to the OMN. We hypothesize that the cMRF, and the SVBNs in particular, play a critical role in the generation of disjunctive saccades. We further hypothesize that projections between the cMRF and SOA form part of a previously undescribed neural circuit that produces vergence integration, allowing vergence angle to be maintained during fixation. Other anatomical and electrophysiological findings demonstrate that the cerebellum, specifically, the caudal fastigial nucleus and the posterior interposed nucleus, play a role in controlling vergence eye movements in both normal and strabismic individuals. We therefore hypothesize that the cerebellar input to the cMRF/SOA complex helps encode or modulate disjunctive saccades. Guided by these overarching hypotheses, we propose Specific Aims to characterize this neural circuitry. 1. To determine the role of SVBNs and the cMRF in the production of disjunctive saccades; 2. To test the hypothesis that the cMRF/SOA complex is the vergence integrator responsible for maintaining the level of convergence; 3. To determine how the cerebellar projections to the cMRF/SOA circuitry are involved in the generation of disjunctive saccades and vergence eye movements. To test our specific hypotheses, we will use established neurophysiological techniques (electrophysiological recordings, antidromic activation, electrical microstimulation and reversible pharmacological modulation). The overall goal of our project is to substantially increase our understanding of the neural circuitry controlling 3D eye movements in primates, and to broadly impact the oculomotor field, leading to new neurophysiological and modeling approaches. These findings will also provide a critical basis for understanding the absence of precise binocular coordination in eye movement dysfunctions such as strabismus.

项目概要/摘要我们通过分离扫视来查看位于 3D 视觉环境中的目标将目标图像投射到两个中央凹上。每次目光转移之后都会有一个用于视觉分析的注视期，在此期间必须保持新的聚散度水平。大多数研究都集中在电路控制共轭上眼跳，而分离性眼跳和辐散眼运动的神经控制受到的关注较少学习。一些模型表明外展运动神经元发送携带信息的单眼命令每只眼睛控制分离性眼跳。其他模型提出了眼跳-聚散爆发的存在神经元（SVBN）投射到内直肌运动神经元，并且仅在分离性眼跳期间活跃。我们已经确定了这种新型细胞类型，仅在分离性眼跳期间放电，位于中央中脑网状结构（cMRF）位于动眼核（OMN）外侧。电微刺激 CMRF 的这个区域会引起分离性眼跳，而失活会损害聚散凝视保持。最近的解剖学发现表明，与近反应相关的前运动神经元位于在 cMRF 中，它们投射到动眼上运动区 (SOA) 和 OMN。我们假设 cMRF，尤其是 SVBN，在分离性眼跳的产生中发挥着关键作用。我们进一步假设 cMRF 和 SOA 之间的投影构成了先前未描述的神经回路的一部分产生聚散积分，允许在固定期间保持聚散角。其他解剖学电生理学结果表明，小脑，特别是尾顶核和后介入核，在正常和正常情况下控制眼球的辐辏运动中发挥作用斜视个体。因此，我们假设 cMRF/SOA 复合体的小脑输入有助于编码或调节分离性眼跳。在这些总体假设的指导下，我们提出了具体目标来表征这个神经回路。 1. 确定 SVBN 和 cMRF 在生产中的作用分离性眼跳； 2. 检验 cMRF/SOA 复合体是聚散积分器的假设负责维持收敛水平； 3. 确定小脑投射如何 cMRF/SOA 电路参与分离眼跳和辐辏眼的生成动作。为了测试我们的具体假设，我们将使用已建立的神经生理学技术（电生理记录、逆向激活、电微刺激和可逆药理调节）。我们项目的总体目标是大幅增加我们对控制灵长类动物 3D 眼球运动的神经回路，并广泛影响动眼神经领域，导致新的神经生理学和建模方法。这些发现也将为了解斜视等眼球运动功能障碍中缺乏精确的双眼协调。