房水排出功能单元（小梁网-Schlemm’s管）间神经调节机制

TM和SC是产生、调节房水阻力的关键，TM-SC间的协调机制是青光眼研究的热点。我们发现，SC开合受自主神经调控，与TM厚度“协调一致”；VIP是SC开合调节的关键分子。但VIP局部分泌和调控及在TM-SC间作用不明。预实验发现：电刺激交感神经，大鼠TM组织交感神经递质DβH表达上调；原代培养大鼠小梁网细胞，VIP表达阳性；肾上腺素点眼，大鼠TM组织ECM减少，TM增厚。假说：兴奋交感神经，促进TM细胞VIP分泌，SC内皮顺应性改变；抑制ECM分泌，TM细胞间距增加，房水滤过增多，共同使SC开大，TM滤过量与SC开合状态吻合。探讨：交感神经兴奋促进TM表达、分泌VIP及对SC内皮细胞生物效应与机制；抑制TM细胞分泌ECM及对TM-SC间形态变化的影响；POAG与正常人TM-SC自主神经递质及受体差异。从交感神经兴奋引起眼压下降生物效应为切入点，为探讨POAG发病机制及临床治疗提供依据。

TM and SC play an important role in the generation and regulation of aqueous humor resistance. Investigating the coordination mechanism of TM-SC is the core to understand its function. Previous studies revealed that the opening-closing state of SC, which was "consistent" with the thickness of TM, was regulated by autonomic nerve; the neurotransmitter VIP was responsible for SC morphological change, however its local secretion and function within TM-SC remained unknown. Pre-experiment suggested that the expression of sympathetic neurotransmitter DβH in rats was up-regulated by electrical stimulation of cervical sympathetic ganglia; VIP was positively stained in primary rat trabecular meshwork cells; ECM expression was decreased and TM thickness was increased induced by epinephrine. Thus the hypothesis is: Increased sympathetic tone promotes VIP secretion of TM cells, changes SC endothelial compliance; inhibits ECM secretion of TM cells, increases intercellular space between TM cells and aqueous outflow facility, resulting in opening of SC, and the amount of aqueous humor filtered through TM is consistent with the opening-closing state SC. This study aimed to explore the effects and mechanisms of increased sympathetic tone on VIP expression and secretion of TM, SC endothelial cell biology; on ECM secretion of TM and morphological changes of TM-SC; and to identify the differences of autonomic neurotransmitters and receptors in TM-SC between POAG and normal human. We took the IOP reduction effect of increased sympathetic tone as the starting point, provide a new basis for further exploration of the pathogenesis in POAG and clinical treatment.