NEURONAL CIRCUITRY CONTROLLING THE EXTRINSIC EYE MUSCLES

敏感和关键功能的第一道防线 眼睛是眼睑。 这个优雅的结构包含了一套对抗性的 肌肉：眼轮匝肌，它关闭眼睛，和提肌 上睑肌，用来睁开眼睛。 盖子展示了两个基本的 行为。 眨眼，它闭上眼睛保护和传播 泪膜由伴随的眼轮匝肌兴奋引发， 提肌抑制 扫视眼睑运动，其中眼睑补偿 对于垂直扫视，仅仅是提肌的功能。 功能障碍 眼睑运动的结果来自许多疾病状态，包括 眼睑痉挛、格雷夫斯病和瓦伦堡综合征。 此外，本发明还提供了一种方法， 眨眼是学习中CNS机制的重要模型。 那里 然而，令人惊讶的是， 引导盖运动。 因此，我们理解眼睑控制的能力 运动及其在疾病中的损害显著受损。 该提案采用多学科方法来界定这些基本的 盖电路。 具体来说，有助于扫视眼睑的途径 运动，眨眼与定向运动和三叉神经 诱发的眨眼将在猫中进行研究。 运动神经元将通过逆行运输识别，并进一步 其特征在于将逆行识别与 抑制性递质的免疫细胞化学定位。 选择 输入将通过结合顺行性 细胞内逆向应变转运技术 确定眼睑运动神经元。 电子显微镜分析 水平将提供顺行标记终端的识别 在细胞内染色的眼睑运动神经元上形成突触。 评估如何 这些发现与灵长类动物的组织有关， 导致眼球牵开肌丧失的电路变化， 解剖实验将扩展到猕猴， 包括上级直肌运动神经元。 因此，解剖结构和发射器 盖控制电路的特异性将在 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.