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Related Experiment Video

Updated: Jul 15, 2026

Assessment of Perigenital Sensitivity and Prostatic Mast Cell Activation in a Mouse Model of Neonatal Maternal Separation
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Neural upregulation in interstitial cystitis.

Omar Nazif1, Joel M H Teichman, G F Gebhart

  • 1Division of Urology, University of British Columbia, Vancouver, British Columbia, Canada.

Urology
|April 28, 2007
PubMed
Summary

Interstitial cystitis (IC) involves bladder hypersensitivity, pain, urgency, and frequency. Research suggests neural upregulation in chronic cystitis may contribute to persistent symptoms and offers potential new treatment avenues.

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Last Updated: Jul 15, 2026

Assessment of Perigenital Sensitivity and Prostatic Mast Cell Activation in a Mouse Model of Neonatal Maternal Separation
09:49

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11:46

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Published on: April 27, 2014

Area of Science:

  • Urology
  • Neuroscience
  • Inflammation Research

Background:

  • Interstitial cystitis (IC) is a chronic condition characterized by bladder hypersensitivity, urgency, frequency, and pelvic pain.
  • The exact cause of IC remains unknown, but proposed mechanisms include epithelial dysfunction, mast cell activation, and neurogenic inflammation.

Purpose of the Study:

  • To explore the pathophysiologic mechanisms underlying interstitial cystitis (IC).
  • To investigate the role of neural upregulation in the peripheral and central nervous systems in IC.
  • To identify potential therapeutic targets for IC.

Main Methods:

  • Review of proposed pathophysiologic mechanisms in IC.
  • Analysis of animal studies demonstrating gene and protein upregulation in response to cystitis.
  • Examination of the role of adenosine triphosphate (ATP) and purinergic receptors in bladder sensation.

Main Results:

  • Animal models show upregulation of various proteins and genes (e.g., proteinase-activated receptors, beta-nerve growth factor, Fos proteins) in response to noxious stimuli.
  • Bladder distention releases ATP, activating P2X3 receptors, which are crucial for bladder sensation and reflexes.
  • Fos protein upregulation in spinal cord neurons is observed in chemically induced cystitis models, suggesting central neural changes.

Conclusions:

  • Neural upregulation, both peripherally and centrally, is implicated in chronic cystitis and interstitial cystitis.
  • The interplay between neural mechanisms and inflammation in IC etiology requires further investigation.
  • Understanding neural pathways in IC offers promising avenues for developing novel treatments.