The external urethral sphincter (EUS) plays a crucial role in maintaining urinary continence. The activity of the EUS is modulated by bladder and urethra sensory neurons. However, a complete understanding of the somatic or visceral sources that modulate the EUS is lacking. The aims of the present study were to characterize the response of the EUS to perineal skin, genital, rectal, and urethral mechanical stimulation, as well as to determine the peripheral neural pathways of the reflex. EUS reflex electromyographic activity (EMG), innervation of pelvic and perineal structures, and the anatomy of afferent and efferent nerves were determined in anesthetized female rats. The EUS responds to cutaneous as well as genital and rectal stimuli. However, the EUS EMG response is significantly larger when induced by genital stimulation. The dorsal nerve of the clitoris and the cavernous nerve both innervate the distal urethra and the distal vagina, as well as the clitoris and perigenital skin and are the main afferent pathways for the genito-sphincteric reflex. Efferent axons travel through the pudendal nerve and the lumbosacral trunk and converge in the motor branch of the lumbosacral plexus, which innervates the EUS. Because the nerves are located on the vaginal walls, they are susceptible to damage during childbirth. Physiology and anatomy of the different neural pathways that regulate EUS activity are important to consider when inducing nerve damage to create models of urinary incontinence.

BackgroundIn this work, a detailed anatomical description of the ovarian plexus nerve (OPN) in rats is presented. The distribution of the OPN was analyzed by gross anatomy; the features of the superior mesenteric ganglion (SMG) were determined by histological studies; and the localization of the postganglionic neurons innervating the ovary were identified with retrograde tracer.We studied 19 adult cyclic rats of the CIIZ-V strain.ResultsWe found that the right OPN originates from the celiac ganglion, the lumbar ganglion of the sympathetic trunk (LGST) and the SMG. The left OPN originates from the LGST and the anastomotic branch from the splanchnic nerve. The SMG was attached to the inferior vena cava containing sympathetic neurons that innervate the right ovary through the OPN, and which is anatomically single. When the tracer was injected into the right ovary, only the SMG showed positive neurons, while when the tracer was injected into the left ovary, labeled postganglionic neurons were observed in the LGST.ConclusionsThis is the first time that it is reported that the SMG is attached to the inferior vena cava and it is directly related to the right ovary. The neural pathways and sympathetic ganglia involved in the communication between the ovaries and the preganglionic neurons are different in the left and right side.

In rats, axons of external urethral sphincter (EUS) motoneurons travel through the anastomotic branch of the pudendal nerve (ABPD) and anastomotic branch of the lumbosacral trunk (ABLT) and converge in the motor branch of the sacral plexus (MBSP). The aim of the present study was to determine in female rats the contribution of these somatomotor pathways and urethral sensory innervation from the dorsal nerve of the clitoris on urinary continence and voiding. EUS electromyographic (EMG) activity during cystometry, leak point pressure (LPP), and voiding efficiency (VE) were assessed in anesthetized virgin Sprague-Dawley female rats before and after transection of the above nerve branches. Transection of the MBSP eliminated EUS EMG, decreased LPP by 50%, and significantly reduced bladder contraction duration, peak pressure, intercontraction interval, and VE. Transection of the ABPD or ABLT decreased EUS EMG discharge and LPP by 25% but did not affect VE. Transection of the dorsal nerve of the clitoris did not affect LPP but reduced contraction duration, peak pressure, intercontraction interval, and VE. We conclude that somatomotor control of micturition is provided by the MBSP with axons travelling through the ABPD and ABLT. Partial somatomotor urethral denervation induces mild urinary incontinence, whereas partial afferent denervation induces voiding dysfunction. ABPD and ABLT pathways could represent a safeguard ensuring innervation to the EUS in case of upper nerve damage. Detailed knowledge of neuroanatomy and functional innervation of the urethra will enable more accurate animal models of neural development, disease, and dysfunction in the future.

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