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Title
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Possible role of the major pelvic ganglion in the modulation of non-voiding activity in rats
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Author
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Abstract
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| Aims: The existence of a motor-sensory system contributing to bladder sensation is now becoming widely accepted. Although it is clear that the motor component of this system appears to be generated within the bladder wall, recent observations suggest that the mechanisms involved in its modulation may lie outside the wall. The present study was undertaken to gain more insights into the peripheral modulation of non-voiding activity and the role of the major pelvic ganglion. Methods: Male Sprague-Dawley rats anesthetized with urethane were used. The bladder was filled till 60% of the micturition threshold volume. The baseline pressure and the superimposed non-voiding activity were observed before and after consecutive bilateral transections of the hypogastric and pelvic nerves and bilateral ablation of the major pelvic ganglia. Results: Hypogastric and pelvic nerve transection didn't significantly change the baseline pressure and superimposed non-voiding activity. Removal of the major pelvic ganglia resulted into an increased baseline pressure when compared with the control and increased amplitude of the non-voiding contractions when compared with both the decentralized condition (both hypogastric and pelvic nerves transected) and the control. The frequency of the non-voiding contractions wasn't affected. Conclusions: Non-voiding activity during the urine storage phase seems to be modulated at the level of the major pelvic ganglion. This suggests the possibility of local circuits between the bladder and the peripheral ganglia that may be responsible for an inhibitory component influencing non-voiding activity. (C) 2016 Elsevier B.V. All rights reserved. |
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Language
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English
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Source (journal)
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Autonomic neuroscience: basic and clinical. - Amsterdam
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Publication
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Amsterdam
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2016
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ISSN
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1566-0702
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DOI
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10.1016/J.AUTNEU.2016.06.002
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Volume/pages
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198
(2016)
, p. 33-37
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ISI
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000383008000006
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Pubmed ID
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27346248
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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