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Updated: Jun 5, 2026

Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice
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Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice

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A non-anesthetized mouse model for recording sensory urinary bladder activity.

Peter Zvara1, Andrew J Wright, Kristopher Roach

  • 1Department of Surgery, University of Vermont College of Medicine Burlington, VT, USA.

Frontiers in Neurology
|December 29, 2010
PubMed
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This study developed an in vivo awake mouse model for bladder sensory nerve recording. The model successfully measured nerve activity changes during bladder filling and chemical stimulation, demonstrating its utility for studying bladder function.

Area of Science:

  • Neuroscience
  • Urology
  • Physiology

Background:

  • Investigating bladder sensory nerve activity is crucial for understanding bladder function and dysfunction.
  • Existing models often lack the ability to record from awake, conscious animals, limiting real-world applicability.
  • Developing a robust in vivo model is essential for advancing research in bladder pain and overactivity.

Purpose of the Study:

  • To establish a novel in vivo awake mouse model for extracellular bladder sensory nerve recording.
  • To validate the model's ability to capture sensory nerve activity during physiological and chemically induced bladder changes.
  • To assess the role of specific sensory pathways in response to bladder distension and chemical irritation.

Main Methods:

  • A bipolar silver electrode was surgically placed under a postganglionic bladder nerve in awake mice.
Keywords:
conscious mousesensory nervesurinary bladder

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  • Efferent nerve signals were blocked to isolate sensory nerve activity.
  • Continuous intravesical infusion of saline, acetic acid, and capsazepine was used to stimulate the bladder.
  • Extracellular nerve activity was recorded and analyzed in relation to bladder pressure changes.

    • Main Results:

    • Reproducible multifiber sensory nerve recordings were obtained from conscious mice.
    • Bladder filling and acetic acid infusion significantly increased sensory nerve firing frequency and bladder pressure.
    • Acetic acid induced a reduction in the intermicturition interval, accompanied by heightened sensory activity.
    • Capsazepine administration attenuated the pressure and sensory responses to acetic acid, indicating involvement of specific receptors.

    Conclusions:

    • The developed awake mouse model provides a reliable platform for studying bladder sensory neurophysiology.
    • This model allows for the investigation of sensory nerve contributions to bladder disorders like overactivity and pain.
    • The findings highlight the utility of this model for preclinical drug testing and mechanistic studies in urology.