CONTROL OF CONJUNCTIVAL GOBLET CELL MUCOUS PRODUCTION

粘液层构成物理和化学屏障， 保护眼睛表面免受细菌和环境的侮辱。 结膜是粘液层最重要的来源之一。 杯状细胞。杯状细胞粘液分泌可被神经刺激 副交感神经和交感神经对角膜的刺激 杯状细胞。这表明杯状细胞能够对 通过分泌粘液快速应对眼表的外部挑战 以保护眼睛表面。在正常情况下，轻微刺激到 眼表将确保持续的低水平分泌。A更多 严重的刺激，如眼睛创伤，将导致更大的 保护性分泌反应。一种粘蛋白缺乏症，如 麻醉角膜，维生素A缺乏症，晚期干燥性角结膜炎， 干燥综合征，热和碱烧伤会随着崩溃而发生 反射性分泌物。出现故障的原因可能是 刺激神经通路，导致粘液分泌减少， 失去保护层，眼表恶化。在……里面 粘膜过度生产的疾病，一种持续刺激的刺激 眼表会增加神经刺激，从而增加 杯状细胞分泌物。这些疾病包括春季结膜炎， 巨乳头性结膜炎、早期干燥性角结膜炎、粘液性结膜炎 钓鱼综合症和过敏症。因此，该项目的总体目标是 以确定不同神经通路的组成部分 通过研究哪些神经刺激粘液分泌， 神经递质、受体、第二信使和细胞类型 牵涉其中。首先，感官、副交感和交感的作用 神经在刺激结膜杯状细胞黏液分泌时会 调查过了。第二，神经纤维的身份和关系 结膜杯状细胞将被测定。第三，政府官员的角色 前列腺素PGE2在神经刺激杯状细胞分泌中的作用 被探索。体内分泌物实验：大鼠结膜高脚杯 角膜创伤或外用药物会刺激细胞分泌。 兴奋剂的应用。结膜纽扣中的杯状细胞粘蛋白， 会进行组织化学染色和单位面积杯状细胞的数量 算上了。这一数字的下降表明粘液的增加 分泌物。对于体外分泌实验，结膜组织将 被移除并与或不与激动剂一起孵育。粘液分泌物会 用螺旋藻的酶联凝集素测定法测定 凝集素，优先识别杯状细胞分泌 产品。杯状细胞的神经支配将由以下因素决定 免疫荧光标记的共聚焦显微镜 免疫电子显微镜。杯状细胞上的受体将被定位 通过免疫组织化学或放射自显影。常态知识 杯状细胞粘液分泌的神经调节机制 为开发疾病的治疗方法提供科学依据 粘液层。

The mucous layer constitutes a physical and chemical barrier that protects the ocular surface from bacterial and environmental insults. One of the most important sources of the mucous layer is conjunctival goblet cells. Goblet cell mucous secretion can be stimulated by a neural stimulus to the cornea via parasympathetic and sympathetic nerves near goblet cells. This suggests that goblet cells are able to respond rapidly to external challenges to the ocular surface by secreting mucus to protect the eye surface. Under normal conditions, minor stimuli to the ocular surface would ensure a constant low level secretion. A more significant stimulus, such as ocular trauma, would cause a greater protective secretory response. A mucin-deficiency disease such as anesthetic cornea, vitamin A deficiency, late keratoconjunctivitis sicca, Sjogrens syndrome, thermal and alkali burns would occur with a breakdown of reflex secretion. Breakdown could occur because of a dysfunction of the stimulating neural pathways, leading to a decreased mucous secretion, loss of the protective coat and deterioration of the ocular surface. In diseases of mucous overproduction, a constant irritative stimulus to the ocular surface would increase neural stimulation, and thus increase goblet cell secretion. These diseases include vernal conjunctivitis, giant papillary conjunctivitis, early keratoconjunctivitis sicca, mucous fishing syndrome, and atopy. Thus, the overall goal of the project is to determine the components of the different neural pathways that stimulate mucous secretion by investigating which nerves, neurotransmitters, receptors, second messengers and cell types are involved. First, the role of sensory, parasympathetic, and sympathetic nerves in stimulating conjunctival goblet cell mucous secretion will be investigated. Second, the identity and relationship of nerve fibers to conjunctival goblet cells will be determined. Third, the role of the prostaglandin PGE2 in neural stimulation of goblet cell secretion will be explored. For in vivo secretion experiments, rat conjunctival goblet cell secretion will be stimulated by a corneal wound or by topical application of agonists. Goblet cell mucin, in buttons of conjunctiva, will be stained histochemically and the number of goblet cells per area counted. A decrease in this number indicates an increase in mucous secretion. For in vitro secretion experiments, conjunctival tissue will be removed and incubated with or without agonists. Mucous secretion will be measured by an enzyme-linked lectin assay using Helix pomatia agglutinin, which preferentially recognizes goblet cell secretory product. The neural innervation of goblet cells will be determined by confocal microscopy with immunofluorescence labelling and by immunoelectron microscopy. Receptors on goblet cells will be localized by immunohistochemistry or autoradiography. Knowledge of the normal mechanism of neural regulation of goblet cell mucous secretion will provide a scientific basis to develop therapeutic treatments for diseases of the mucous layer.