Somatomotor and sensory urethral control of micturition in female rats

Cruz, Yolanda; Pastelín, C.F.; Balog, Brian; Zaszczurynski, Paul; Damaser, Margot S.

doi:10.1152/ajprenal.00255.2014

Cited by 14 publications

(15 citation statements)

References 47 publications

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“…Voiding duration in DNI awake rats increased, contrary to the decreased contraction duration observed in anesthetized animals 9 . Contrary results may indicate that in awake condition, DNI induced decrement in excitatory urethrabladder reflexes for positive bladder feedback during voiding 8 may be compensated by other mechanisms that contributes to urine expulsion, such as abdominal straining at desire to void described in voiding dysfunction patients 18 , but void may require longer time.…”

Section: Accepted Manuscriptcontrasting

confidence: 62%

“…previous results demonstrated that in anesthetized rats bilateral transection of the sensory branch of the pudendal nerve, also known as DN, dramatically reduced voiding intervals, bladder contraction duration and voiding volume 8,9 , suggesting that afferents travelling through DN are important pathways of excitatory urethrabladder reflexes triggered in response to urine flux during voiding 8,9 . Electrical stimulation of the DN proximal to the transection significantly improved voiding efficiency, supporting the idea of a positive modulation of the bladder via the pudendal nerve 5 .…”

Section: Moderate Effect Of Dni On Micturition Parameters Was Unexpecmentioning

confidence: 97%

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Coital Urinary Incontinence Induced by Impairment of the Dorsal Nerve of the Clitoris in Rats

et al. 2016

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Section: Accepted Manuscriptcontrasting

confidence: 62%

Section: Moderate Effect Of Dni On Micturition Parameters Was Unexpecmentioning

confidence: 97%

Coital Urinary Incontinence Induced by Impairment of the Dorsal Nerve of the Clitoris in Rats

et al. 2016

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“…Stretching nerve injury may also decrease microtubules and tau protein, important elements in axonal function (51). DNC and MBSP stretching due to VD may induce sexual and urinary dysfunction, since denervation of the clitoris induces signs of coital urinary incontinence (5) and damage of the EUS innervation induced signs of urinary incontinence in rats (6,29,42).…”

Section: 56)mentioning

confidence: 99%

Neuroanatomic and behavioral correlates of urinary dysfunction induced by vaginal distension in rats

Palacios-Galicia

Juárez

Morán

et al. 2016

American Journal of Physiology-Renal Physiology

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-The aim of the present study was to use a model of simulated human childbirth in rats to determine the damage to genitourinary structures and behavioral signs of urinary dysfunction induced by vaginal distension (VD) in female rats. In experiment 1, the length of the genitourinary tract and the nerves associated with it were measured immediately after simulated human delivery induced by VD or sham (SH) procedures. Electroneurograms of the dorsal nerve of the clitoris (DNC) were also recorded. In experiment 2, histological characteristics of the bladder and major pelvic ganglion of VD and SH rats were evaluated. In experiment 3, urinary parameters were determined in conscious animals during 6 h of dark and 6 h of light before and 3 days after VD or SH procedures. VD significantly increased distal vagina width (P Ͻ 0.001) and the length of the motor branch of the sacral plexus (P Ͻ 0.05), DNC (P Ͻ 0.05), and vesical nerves (P Ͻ 0.01) and decreased DNC frequency and amplitude of firing. VD occluded the pelvic urethra, inducing urinary retention, hematomas in the bladder, and thinness of the epithelial (P Ͻ 0.05) and detrusor (P Ͻ 0.01) layers of the bladder. Major pelvic ganglion parameters were not modified after VD. Rats dripped urine in unusual places to void, without the stereotyped behavior of micturition after VD. The neuroanatomic injuries after VD occur alongside behavioral signs of urinary incontinence as determined by a new behavioral tool for assessing micturition in conscious animals. external urethral sphincter; dorsal nerve of the clitoris; major pelvic ganglion; micturition MICTURITION consists of two phases: storage and urine expulsion. During storage, the detrusor is relaxed while the bladder neck and urethra are activated, preventing involuntary bladder emptying (11). Extrinsic elements such as the levator ani muscle also contribute to the maintenance of continence (3). When the bladder reaches its threshold volume, spinal and supraspinal reflexes are triggered to induce bladder contraction and urethral relaxation, and urine flows through the urethra (11). Damage to the lower urinary tract and/or its innervation can induce urinary dysfunction (3,29,41).Urinary dysfunction affects the health of many women (60). Stress urinary incontinence has been described as involuntary loss of urine during effort and is the most prevalent urinary disorder related to vaginal childbirth, which is known to injure the pudendal nerve and denervate the external urethral sphincter (EUS) (3, 15, 57).Maternal pelvic viscera and nerve damage results from the difficulty of human childbirth due the large fetal head and brain relative to the maternal pelvis size. Neonates at birth have heads that are close to the size of the maternal birth canal through which they must pass during the second stage of parturition (48). Births of fetuses over 4 kg or fetal malposition often prolong parturition (30), retaining the fetus in the pelvic cavity, the main anatomic resistance to fetal expulsion. Prolonged second stage of parturition...

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“…Electrical signals in the EUS were significantly impaired after 4 weeks, and intravesical inhibition of P2X2/3R remarkably attenuated EUS responsiveness during voiding contractions. This is very interesting, as the innervation to the urethra is provided by the pudendal nerve, which has different functions than those from the pelvic or hypogastric nerves, and conveys afferent and efferent information from the EUS to the CNS [9,31,32]. Although the pudendal nerve shares its origin with the pelvic nerve at the L6-S1 spinal segments of the rat [31,32], it is important to consider that in our present SCI model, both the dorsal roots and dorsal horn sensory neurones may be mostly affected by the impact.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, motor unit activation patterns in the EUS of a SCI rat can be activated at low, medium or high-pressure thresholds, indicating the loss of LUT synergy and regulatory complications associated with the injury [8]. Other studies have provided a working idea of how pelvic innervation regulates activity in the EUS and detrusor contraction during CMG; therefore unmasking to what extent an SCI can devastate LUT regulation [9,10]. In the same sense, a very relevant and recent observation was made that illustrated the ability of LUT afferent pathways to generate hyper-excitable conditions after SCI in rodents.…”

Section: Introductionmentioning

confidence: 99%

Modulatory effects of intravesical P2X2/3 purinergic receptor inhibition on lower urinary tract electromyographic properties and voiding function of female rats with moderate or severe spinal cord injury

et al. 2018

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Objectives To evaluate the role that intravesical P2X2/3 purinergic receptors (P2X2/3Rs) play in early and advanced neurogenic lower urinary tract (LUT) dysfunction after contusion spinal cord injury (SCI) in female rats. Materials and Methods Female Sprague‐Dawley rats received a thoracic Th8/Th9 spinal cord contusion with either force of 100 kDy (cN); moderate) or 150 kDy (cN; severe); Sham rats had no injury. Evaluations on urethane‐anesthetised rats were conducted at either 2 or 4 weeks after SCI. LUT electrical signals and changes in bladder pressure were simultaneously recorded using cystometry and a set of custom‐made flexible microelectrodes, before and after intravesical application of the P2X2/3R antagonist AF‐353 (10 μM), to determine the contribution of P2X2/3R‐mediated LUT modulation. Results Severe SCI significantly increased bladder contraction frequency, and reduced both bladder pressure amplitude and intraluminal‐pressure high‐frequency oscillations (IPHFO). Intravesical P2X2/3R inhibition did not modify bladder pressure or IPHFO in the Sham and moderate‐SCI rats, although did increase the intercontractile interval (ICI). At 2 weeks after SCI, the Sham and moderate‐SCI rats had significant LUT electromyographic activity during voiding, with a noticeable reduction in LUT electrical signals seen at 4 weeks after SCI. Intravesical inhibition of P2X2/3R increased the ICI in the Sham and moderate‐SCI rats at both time‐points, but had no effect on rats with severe SCI. The external urethral sphincter (EUS) showed strong and P2X2/3R‐independent electrical signals in the Sham and moderate‐SCI rats in the early SCI stage. At 4 weeks after SCI, the responsiveness of the EUS was significantly attenuated, independently of SCI intensity. Conclusions This study shows that electrophysiological properties of the LUT are progressively impaired depending on SCI intensity and that intravesical P2X2/3R inhibition can attenuate electrical activity in the neurogenic LUT at early, but not at semi‐chronic SCI. This translational study should be useful for planning clinical evaluations.

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Somatomotor and sensory urethral control of micturition in female rats

Cited by 14 publications

References 47 publications

Coital Urinary Incontinence Induced by Impairment of the Dorsal Nerve of the Clitoris in Rats

Coital Urinary Incontinence Induced by Impairment of the Dorsal Nerve of the Clitoris in Rats

Neuroanatomic and behavioral correlates of urinary dysfunction induced by vaginal distension in rats

Modulatory effects of intravesical P2X2/3 purinergic receptor inhibition on lower urinary tract electromyographic properties and voiding function of female rats with moderate or severe spinal cord injury

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