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Related Experiment Video

Updated: Sep 8, 2025

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TGR5 agonists induce peripheral and central hypersensitivity to bladder distension.

Ashlee Caldwell1,2,3, Luke Grundy1,2, Andrea M Harrington1,2

  • 1Visceral Pain Research Group, College of Medicine and Public Health, Flinders Health and Medical Research Institute (FHMRI), Flinders University, Bedford Park, South Australia, 5042, Australia.

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|June 15, 2022
PubMed
Summary

The bile acid receptor TGR5 (Gpbar1) is expressed in mouse bladders and nerves. TGR5 activation enhances bladder sensitivity, suggesting its role in conditions like interstitial cystitis/bladder pain syndrome (IC/BPS) and overactive bladder syndrome (OAB).

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Area of Science:

  • Urology
  • Neuroscience
  • Gastroenterology

Background:

  • Chronic bladder conditions like IC/BPS and OAB have unclear mechanisms.
  • Neuronal hypersensitivity is a key factor in these conditions.
  • TGR5, a bile acid receptor, is implicated in visceral neuronal hypersensitivity.

Purpose of the Study:

  • To investigate the role of TGR5 in bladder afferent sensitivity.
  • To determine if TGR5 is expressed in bladder-innervating neurons.
  • To assess the impact of TGR5 activation on bladder mechanosensitivity.

Main Methods:

  • Examined TGR5 (Gpbar1) mRNA expression in mouse bladders and dorsal root ganglia (DRG).
  • Performed in vitro calcium imaging of bladder-innervating DRG neurons stimulated with TGR5 agonists.
  • Utilized ex vivo and in vivo mouse models to measure bladder afferent mechanosensitivity and spinal dorsal horn neuronal activation.

Main Results:

  • TGR5 mRNA was found in all bladder layers and in bladder-innervating DRG neurons, co-expressed with Trpv1 and Trpa1.
  • TGR5 agonists directly activated bladder-innervating DRG neurons, an effect dependent on Trpv1.
  • Activation of TGR5 enhanced bladder afferent mechanosensitivity and spinal dorsal horn neuronal activation in a Gpbar1-dependent manner.

Conclusions:

  • TGR5 plays a significant role in mediating bladder afferent hypersensitivity to distension.
  • TGR5 may be a potential therapeutic target for managing symptoms of IC/BPS and OAB.