SUPRAPONTINE CONTROL OF MICTURITION

尿液的储存和定期释放是从几个层面控制的 包括腰骶脊髓在内的中枢神经系统 脑桥吻侧、下丘脑、许多皮质下核团和大脑 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 起源于脑桥喙部并将纤维发送到骶脊髓 线. 脑桥区域尾部的中枢神经系统受损 会导致严重的尿潴留 临床研究也表明， 由于中风、肿瘤、创伤或 中枢神经系统疾病在某些情况下会导致 高活动性膀胱伴尿急和尿失禁，在其他情况下， 膀胱功能减退伴尿潴留。 本提案中概述的研究旨在提供一个 详细的分析，使用现代神经解剖学和神经生理学 技术，调节神经元活动的脑桥上结构 排尿反射路径的一部分 本研究的主要目的是：（1）确定 用辣根过氧化物酶示踪技术的中枢神经系统 其向脑桥排尿中心（PMC）（2）提供直接输入， 识别介导PMC输入的可能的神经递质; 脑啡肽、血清素、去甲肾上腺素、P物质和乙酰胆碱将 特别感兴趣（3）记录PMC的诱发电位， 骨盆神经刺激，并检查刺激的调节作用 不同的前脑结构（4），以阻止特定的神经递质 拮抗剂或用激动剂模拟上述调节作用 上述（5）使用5个barelled细胞检查PMC的单个神经元 微电极，并确定所用药物的效果 离子电渗作用于这些神经元。 本研究中获得的信息 将不仅提供一个更完整的布线图， 排尿途径，但也可能表明可能的药理学 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.