scholarly journals Psychological stress induced bladder overactivity in female mice is associated with enhanced afferent nerve activity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kylie A. Mills ◽  
Eliza G. West ◽  
Donna J. Sellers ◽  
Russ Chess-Williams ◽  
Catherine McDermott

AbstractPsychological stress has been linked to the development and exacerbation of overactive bladder symptoms, as well as afferent sensitisation in other organ systems. Therefore, we aimed to investigate the effects of water avoidance stress on bladder afferent nerve activity in response to bladder filling and pharmaceutical stimulation with carbachol and ATP in mice. Adult female C57BL/6J mice were exposed to either water avoidance stress (WAS) for 1 h/day for 10 days or normal housing conditions. Voiding behaviour was measured before starting and 24-h after final stress exposure and then animals were euthanised to measure afferent nerve activity in association with bladder compliance, spontaneous phasic activity, contractile responses, as well as release of urothelial mediators. WAS caused increased urinary frequency without affecting urine production. The afferent nerve activity at low bladder pressures (4–7 mmHg), relevant to normal physiological filling, was significantly increased after stress. Both low and high threshold nerves demonstrated enhanced activity at physiological bladder pressures. Urothelial ATP and acetylcholine release and bladder compliance were unaffected by stress as was the detrusor response to ATP (1 mM) and carbachol (1 µM). WAS caused enhanced activity of individual afferent nerve fibres in response bladder distension. The enhanced activity was seen in both low and high threshold nerves suggesting that stressed animals may experience enhanced bladder filling sensations at lower bladder volumes as well as increased pain sensations, both potentially contributing to the increased urinary frequency seen after stress.

2015 ◽  
Vol 309 (6) ◽  
pp. R629-R638 ◽  
Author(s):  
Gerald C. Mingin ◽  
Thomas J. Heppner ◽  
Nathan R. Tykocki ◽  
Cuixia Shi Erickson ◽  
Margaret A. Vizzard ◽  
...  

Social stress has been implicated as a cause of urinary bladder hypertrophy and dysfunction in humans. Using a murine model of social stress, we and others have shown that social stress leads to bladder overactivity. Here, we show that social stress leads to bladder overactivity, increased bladder compliance, and increased afferent nerve activity. In the social stress paradigm, 6-wk-old male C57BL/6 mice were exposed for a total of 2 wk, via barrier cage, to a C57BL/6 retired breeder aggressor mouse. We performed conscious cystometry with and without intravesical infusion of the TRPV1 inhibitor capsazepine, and measured pressure-volume relationships and afferent nerve activity during bladder filling using an ex vivo bladder model. Stress leads to a decrease in intermicturition interval and void volume in vivo, which was restored by capsazepine. Ex vivo studies demonstrated that at low pressures, bladder compliance and afferent activity were elevated in stressed bladders compared with unstressed bladders. Capsazepine did not significantly change afferent activity in unstressed mice, but significantly decreased afferent activity at all pressures in stressed bladders. Immunohistochemistry revealed that TRPV1 colocalizes with CGRP to stain nerve fibers in unstressed bladders. Colocalization significantly increased along the same nerve fibers in the stressed bladders. Our results support the concept that social stress induces TRPV1-dependent afferent nerve activity, ultimately leading to the development of overactive bladder symptoms.


2016 ◽  
pp. 341-348 ◽  
Author(s):  
M. CHOUDHARY ◽  
F. CLAVICA ◽  
R. VAN MASTRIGT ◽  
E. VAN ASSELT

Electrophysiological studies of whole organ systems in vitro often require measurement of nerve activity and/or stimulation of the organ via the associated nerves. Currently two-compartment setups are used for such studies. These setups are complicated and require two fluids in two separate compartments and stretching the nerve across one chamber to the other, which may damage the nerves. We aimed at developing a simple single compartment setup by testing the electrophysiological properties of FC-770 (a perfluorocarbon) for in vitro recording of bladder afferent nerve activity and electrical stimulation of the bladder. Perflurocarbons are especially suitable for such a setup because of their high oxygen carrying capacity and insulating properties. In male Wistar rats, afferent nerve activity was recorded from postganglionic branches of the pelvic nerve in vitro, in situ and in vivo. The bladder was stimulated electrically via the efferent nerves. Organ viability was monitored by recording spontaneous contractions of the bladder. Additionally, histological examinations were done to test the effect of FC-770 on the bladder tissue. Afferent nerve activity was successfully recorded in a total of 11 rats. The bladders were stimulated electrically and high amplitude contractions were evoked. Histological examinations and monitoring of spontaneous contractions showed that FC-770 maintained organ viability and did not cause damage to the tissue. We have shown that FC-770 enables a simple, one compartment in vitro alternative for the generally used two compartment setups for whole organ electrophysiological studies.


1999 ◽  
Vol 276 (6) ◽  
pp. R1819-R1824
Author(s):  
Els van Asselt ◽  
Joost le Feber ◽  
Ron van Mastrigt

In this study, the mechanism involved in the initiation of voiding was investigated. Bladder pressure and bladder and urethral nerve activity were recorded in the anesthetized rat. Bladder nerve activity was resolved into afferent and efferent activity by means of a theoretical model. The beginning of an active bladder contraction was defined as the onset of bladder efferent firing at a certain time ( t 0). From t 0 onward, bladder efferent activity increased linearly during δ t seconds (rise time) to a maximum. The pressure at t 0 was 1.0 ± 0.4 kPa, the afferent nerve activity at t 0 was 2.0 ± 0.6 μV (53 ± 15% of maximum total nerve activity), and δ t was 11 ± 13 s. Between contractions the afferent activity at t 0 was never exceeded. Urethral afferent nerve activity started at bladder pressures of 2.1 ± 1.1 kPa. Therefore, we concluded that urethral afferent nerve activity does not play a role in the initiation of bladder contractions; voiding contractions presumably are initiated by bladder afferent nerve activity exceeding a certain threshold.


1999 ◽  
Vol 162 (1) ◽  
pp. 204-212 ◽  
Author(s):  
SUK YOUNG JUNG ◽  
MATTHEW O. FRASER ◽  
HIDEO OZAWA ◽  
OSAMU YOKOYAMA ◽  
MITSUHARU YOSHIYAMA ◽  
...  

2007 ◽  
Vol 27 (7) ◽  
pp. 1725-1737 ◽  
Author(s):  
E. Erazo-Fischer ◽  
J. Striessnig ◽  
H. Taschenberger

2019 ◽  
Vol 18 (6) ◽  
pp. 1915-1926 ◽  
Author(s):  
Lingxia Bao ◽  
Jingbo Zhao ◽  
Donghua Liao ◽  
Guixue Wang ◽  
Hans Gregersen

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