SUPRAPONTINE CONTROL OF MICTURITION

尿液的储存和定期释放受到多个层面的控制 中枢神经系统，包括腰椎脊髓， 脑桥、下丘脑、大量皮质下核团和大脑 大脑皮层。各种证据表明，兴奋性副交感神经 排尿反射的成分依赖于脊髓上通路 起源于吻侧脑桥，并将纤维发送到骶髓 电源线。脑桥区尾侧中枢神经系统受损 会导致严重的尿滞留。临床研究也表明， 无论是由于中风、肿瘤、骨膜瘤或其他原因造成的尖端结构损伤 中枢神经系统疾病在某些情况下可导致 膀胱过度活动，有紧迫感和大小便失禁，在其他情况下 膀胱活动减退伴尿滞留。 本提案中概述的研究旨在提供一个 运用现代神经解剖学和神经生理学进行详细分析 桥上结构调节神经元活动的技术 排尿反射通路。 这项拟议研究的目的是：(1)在 用辣根过氧化物酶示踪技术追踪中枢神经系统 其向脑桥排尿中心(PMC)(2)提供直接输入以 确定可能的神经递质，这些神经递质调节PMC的输入； 脑啡肽、5-羟色胺、去甲肾上腺素、P物质和去乙酰胆碱 特别感兴趣的是(3)记录从PMC到 盆腔神经刺激并检测刺激的调节作用 用特定的神经递质阻断各种前脑结构(4) 自激动剂或用激动剂模拟上述的调节影响 上面(5)用五个支架检查PMC的单个神经元 微电极和确定所用药物的效果 以离子电泳法连接到这些神经元。从这项研究中获得的信息 不仅将提供更完整的接线图， 排尿途径，但也可能提示可能的药理学 排尿行为的改变。

The storage and periodic release of urine is controlled from several levels of the central nervous system, including the lumbosacral spinal cord, rostral pons, hypothalamus, numerous subcortical nuclei, and the cerebral cortex. Various evidence indicates that the excitatory parasympathetic component of the micturition reflex is dependent upon a supraspinal pathway originating in the rostral pons and sending fibers to the sacral spinal cord. Damage to the central nervous system caudal to this pontine area causes profound urinary retention. Clinical studies have also shown that damage to supropointine structures whether due to stroke, tumors, trama, or disease of the central nervous system can cause in some instances a huperactive bladder with urgency and incontinence and in other instances a hypoactive bladder with urinary retention. The studies outlined in the present proposal are designed to provide a detailed analysis, using modern neuroanatomical and neurophysiological techniques, of suprapontine structures which modulate the neuronal activity of the micturition reflex pathway. The aims of this proposed research are: (1) to identify site in the central nervous system using horseradish peroxidase tracting techniques which provide direct input to pontine micturition center (PMC) (2) to identify possible neurotransmitters which mediate the input to the PMC; enkephalins, serotonin, norepinephrine, substanace P and aaetylcholine will be of particular interest (3) to record evoked potentials from the PMC to pelvic nerve stimulation and examine the modulatory effects of stimulation of various forebrain structure (4) to block with specific neurotransmitter antogonists or mimic with agonists the modulatory influences mentioned above (5) to examine single neurons of the PMC using five barelled mocroelectrodes and to determine the effects of drugs applied iontophoretically to these neurons. The information gained in this study will not only provide a much more complete wiring diagram for the micturition pathway but may also suggest possible pharmacological modifications of the act of micturition.