CORNEAL NEUROBIOLOGY

拟议的研究将扩展该实验室以前的发现 来扩展我们对代谢和生理的理解 角膜的神经支配与角膜上皮的关系 上皮 以前开发的定量，解剖， 用于评估的结构和功能方面的生理学方法 感觉神经支配将被应用于理解 众所周知，但知之甚少的角膜减少的原因 由于接触透镜佩戴和糖尿病引起的敏感性。 角膜 将在兔子中研究配戴接触透镜后的敏感性变化。 这项工作的目的是确定隐形眼镜如何影响 角膜中的感觉传递。 通过注射 将在不同的时间间隔通过光检查链脲霉素， 电子显微镜检查以确定神经变性的过程。 对糖尿病患者的心理物理学研究将与 角膜敏感性与其他神经系统变化，以确定是否 角膜可以提供一个独特的窗口，早期感觉神经的变化， 糖尿病人 其他研究将确定放射性标记的 物质从三叉神经节轴浆运输到三叉神经节 角膜上皮，以及这些材料可能成为 上皮细胞可以利用。 神经再生 将检查穿透性角膜移植术，以确定 恢复正常的角膜神经系统。 将决定是否 上皮细胞中存在高和低亲和力的胆碱摄取系统， 细胞;此外，角膜的特定去神经支配的影响和变化 在上皮细胞有丝分裂活动中，例如在伤口愈合中， 将研究系统。 电生理学研究将允许 角膜感觉神经的解剖学和生理学相关性 受体通过三叉神经节细胞的细胞内记录， 随后注射轴浆运输示踪剂。 还有， 面向伤口的侧枝芽的感觉能力将 评估对机械、热和化学刺激的反应。 它 可能是在响应参数中看到的变化类型 特征将产生一些深入了解参与的机制， 与角膜损伤相关的异常感觉的产生。 从这些研究中获得的信息可能会导致开发新的 加速角膜伤口愈合的治疗方法。

The proposed studies will extend the previous findings of this laboratory to expand our understanding of the metabolic and physiological relationships between the innervation of the cornea and the corneal epithelium. Previously developed quantitative, anatomical, and physiological methods for assessing structural and functional aspects of the sensory innervation will be applied to understanding the underlying causes of the well-known, but poorly understood decreased corneal sensitivity attributed to contact lens wear and to diabetes. Corneal sensitivity changes after contact lens wear will be studied in the rabbit. The object of this work will be to determine how contact lenses affect sensory transmission in the cornea. Rats made diabetic by injection of streptozotocin will be examined at various intervals by means of light and electron microscopy to determine the course of neural degeneration. Psychophysical studies of diabetic patients will correlate changes in corneal sensitivity with other neurological changes to determine if the cornea could provide a unique window into early sensory nerve changes in diabetics. Other studies will determine the fate of radiolabeled substances axoplasmically transported from the trigeminal ganglion to the corneal epithelium, and the routes by which these materials could become available to the epithelial cells. Nerve regeneration following penetrating keratoplasty will be examined to identify the barriers to restoration of the normal corneal neurology. It will be determined whether both high- and low-affinity systems exist for choline uptake in epithelial cells; also, the effects of specific denervation of the cornea and changes in epithelial mitotic activity, such as in wound healing, on the choline uptake system will be studied. Electrophysiological studies will permit the correlation of the anatomy and physiology of the corneal sensory receptors by intracellular recording from trigeminal ganglion cells, followed by the injection of an axoplasmically-transported tracer. Also, the sensory capabilities of wound-oriented collateral sprouts will be assessed in response to mechanical, thermal, and chemical stimulation. It may be that the types of changes seen in the parameters of the response characteristics will yield some insight into the mechanisms involved in the production of the abnormal sensations associated with corneal injury. Information from these studies could lead to the development of new therapeutic methods for accelerating corneal wound healing.