PAIN IN THE CORNEA

角膜上皮痛觉感受器的传导机制 将通过电生理学、药理学和 心理物理技术。 各种刺激之间的相互作用 模态，例如，触摸，渗透压和温度，将被测试 进行总结和交叉适应，以检查它们是否共享路径。 从上皮细胞释放的化学递质的干预 细胞，将通过测试活性剂的影响来寻找， 他们的抑制剂在接收阈值上。 的灌注液， 将检查离体角膜是否有释放的直接证据。 发射器对整个角膜表面的刺激。 发射机 被研究的药物包括乙酰胆碱、钾和激肽。 将 需要知道受体处的药剂浓度 终端，和一个附属项目将是确定的动态 溶质通过上皮细胞旁间隙的转移，以及 这将受到细胞摄取或酶分解的影响， 溶质 长期使用局部麻醉剂会导致角膜溃疡， 并通过低浓度持续灌流研究其作用机制 在角膜表面或局部进入基质。 变化 在角膜上皮的功能和结构上， 去神经支配后将被寻找。 轴突运输的证据 三叉神经将被寻找，如果找到了， 并记录了对角膜的影响。 将尝试 以测试局部麻醉是否会导致轴突中断 运输

The transduction mechanism of the pain receptor in the corneal epithelium will be examined by electrophysiological, pharamacological and psychophysical techniques. Interaction between various stimulation modalities, e.g., touch, osmotic pressure and temperature, will be tested for summation and cross adaptation to examine whether they share pathways. The intervention of a chemical transmitter, liberated from the epithelial cells, will be looked for by testing the influence of active agents and their inhibitors on the threshold of reception. The perfusate of the isolated cornea will be examined for direct evidence of release of transmitter on stimulation of the entire corneal surface. Transmitters to be studied include acetylcholine, potassium and kinins. It will be necessary to know the concentration of the agents at the receptor terminals, and a subsidiary project will be to determine the dynamics of solute transfer through the paracellular spaces of the epithelium and how this would be affected by cellular uptake or enzymatic breakdown of the solute. Prolonged use of local anesthetics leads to corneal ulceration, and the mechanism will be studied by the continuous perfusion of low levels of anesthetic over the corneal surface or locally into the stroma. Changes in function and structure of the corneal eptielium similar to those following denervation will be looked for. Evidence of axonal transport in the trigeminal nerve will be sought, and if it is found attempts will be made to block it and the effect on the cornea noted. An attempt will be made to test if local anesthesia results in an interruption of axonal transport.