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Neural pathways of somatic and visceral reflexes of the external urethral sphincter in female rats
Author(s) -
Pastelín C.F.,
Juárez R.,
Damaser M.S.,
Cruz Y.
Publication year - 2012
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.23079
Subject(s) - pudendal nerve , clitoris , external anal sphincter , anatomy , urethra , reflex , efferent , urethral sphincter , stimulation , biology , medicine , neuroscience , afferent , anal canal , rectum
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. J. Comp. Neurol., 520:3120–3134, 2012. © 2012 Wiley Periodicals, Inc.