NEURONAL CIRCUITRY CONTROLLING THE EXTRINSIC EYE MUSCLES

的敏感和关键职能的第一道防线 眼睛就是眼皮。这种优雅的结构包含了一套对抗性的 肌肉：闭眼的眼轮匝肌和提肌 掌上肌，开眼界。这个盖子有两个基本特征 行为。闭上眼睛保护眼睛并散开的眨眼 泪膜是由伴随的眼轮匝肌兴奋和 提肌抑制。眼跳式的眼盖运动，在这种运动中，眼盖可以补偿 对于垂直扫视，仅是提升器的一个功能。功能障碍 由多种疾病状态导致的盖子运动，包括 眼睑痉挛、格雷夫病和瓦伦堡综合征。此外, 瞬目是中枢神经系统学习机制的重要模型。那里 然而，令人惊讶的是，人们对基本的神经回路知之甚少 指导盖子的运动。因此，我们了解盖子控制的能力 运动及其在疾病中的损害严重受损。 本提案采用多学科方法来定义这些基本的 盖子电路。具体地说，俯视眼球盖的路径 运动，与定向运动和三叉神经相关的眨眼 我们将对猫的眨眼行为进行调查。对盖子的假定输入 运动神经元将通过逆行运输进行识别，并进一步 其特点是将逆行鉴定与 抑制性递质的免疫细胞化学定位。已选择 输入将通过结合顺行线进行明确演示 逆流胞内应变输送技术 识别出了盖子运动神经元。用电子显微镜进行分析 水平将提供顺向标记的终末的标识 细胞内染色的盖运动神经元上的突触。评估如何 这些发现与灵长类组织有关，并确定了 导致眼球拉直肌丧失的回路变化， 解剖学实验将扩展到猕猴和 包括上直肌运动神经元。因此，解剖学和传播学 盖子控制电路的特性将在 功能上下文。

The first line of defense for the sensitive and critical functions of the eye is the eyelid. This elegant structure contains a set of antagonistic muscles: the orbicularis oculi, which closes the eye, and the levator palprebrae superioris, which opens the eye. The lid exhibits two basic behaviors. The blink, which closes the eye for protection and spreads the tear film, is initiated by concomitant orbicularis excitation and levator inhibition. Saccadic lid movements, in which the lid compensates for vertical saccades, are solely a function of the levator. Dysfunction of lid movement results from numerous disease states, including blepharospasm, Grave's disease and Wallenberg's syndrome. In addition, the blink is an important model for CNS mechanisms in learning. There is, however, surprisingly little known about the basic neural circuits directing lid movements. Thus, our capacity to understand control of lid movement and its impairment in disease is significantly compromised. This proposal applies a multidisciplinary approach to define these basic lid circuits. Specifically, the pathways that subserve saccadic lid movements, blinks associated with orienting movements and trigeminally evoked blinks will be investigated in the cat. Putative inputs to lid motoneurons will be identified via retrograde transport and further characterized by combining retrograde identification with immunocytochemical localization of inhibitory transmitters. Selected inputs will be definitively demonstrated by combining anterograde transport techniques with the intracellular straining of antidromically identified lid motoneurons. Analysis using the electron microscopic level will provide identification of anterogradely labelled terminals synapsing on intracellularly stained lid motoneurons. To assess how these findings relate to the primate organization and identify the circuitry changes that underlie the loss of the retractor bulbi muscles, the anatomical experiments will be extended to macaque monkeys and include superior rectus motoneurons. Thus, the anatomy and transmitter specificity of the lid control circuitry will be determined in a functional context.