Department of Pharmacology and Chemical Biology, University of Pittsburgh Medical School, Pittsburgh, PA 15261, USA.
Exp Neurol. 2012 May;235(1):123-32. doi: 10.1016/j.expneurol.2011.05.003. Epub 2011 May 9.
The lower urinary tract has two main functions, storage and periodic expulsion of urine, that are regulated by a complex neural control system in the brain and lumbosacral spinal cord. This neural system coordinates the activity of two functional units in the lower urinary tract: (1) a reservoir (the urinary bladder) and (2) an outlet (consisting of bladder neck, urethra and striated muscles of the external urethra sphincter). During urine storage the outlet is closed and the bladder is quiescent to maintain a low intravesical pressure. During micturition the outlet relaxes and the bladder contracts to promote efficient release of urine. This reciprocal relationship between bladder and outlet is generated by reflex circuits some of which are under voluntary control. Experimental studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through a coordination center (the pontine micturition center) located in the rostral brainstem. This reflex pathway is in turn modulated by higher centers in the cerebral cortex that are involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary control of voiding as well as the normal reflex pathways that coordinate bladder and sphincter function. Following spinal cord injury the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. However the bladder does not empty efficiently because coordination between the bladder and urethral outlet is lost. Studies in animals indicate that dysfunction of the lower urinary tract after spinal cord injury is dependent in part on plasticity of bladder afferent pathways as well as reorganization of synaptic connections in the spinal cord. Reflex plasticity is associated with changes in the properties of ion channels and electrical excitability of afferent neurons and appears to be mediated in part by neurotrophic factors released in the spinal cord and/or the peripheral target organs.
下尿路有两个主要功能，储存和周期性排空尿液，这两个功能由大脑和腰骶脊髓中的复杂神经控制系统调节。该神经系统协调下尿路的两个功能单位的活动：（1）储尿器（膀胱）和（2）出口（由膀胱颈部、尿道和外尿道横纹肌括约肌组成）。在储尿期间，出口关闭，膀胱处于静止状态以维持低膀胱内压。在排尿期间，出口放松，膀胱收缩以促进尿液的有效释放。膀胱和出口之间的这种相互关系是由反射回路产生的，其中一些是在自愿控制下。动物实验研究表明，排尿反射是由通过位于脑干前部的协调中心（桥脑排尿中心）的脊髓-延髓反射通路介导的。该反射通路反过来又受到大脑皮层中参与排尿自愿控制的高级中枢的调制。颈段或胸段脊髓损伤会破坏排尿的自主控制以及协调膀胱和括约肌功能的正常反射通路。脊髓损伤后，膀胱最初是无反射的，但随后由于出现脊髓排尿反射通路而变得反射亢进。然而，由于膀胱和尿道出口之间的协调丧失，膀胱不能有效地排空。动物研究表明，脊髓损伤后下尿路功能障碍部分取决于膀胱传入途径的可塑性以及脊髓中突触连接的重组。反射可塑性与传入神经元的离子通道特性和电兴奋性的变化有关，并且似乎部分由脊髓和/或周围靶器官释放的神经营养因子介导。
