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The Use of Cystometry in Small Rodents: A Study of Bladder Chemosensation
Published on: August 21, 2012
Function of the Cold Receptor (TRPM8) Associated with Voiding Dysfunction in Bladder Outlet Obstruction in Rats
Ji Hee Jun1, Hyo Jin Kang, Mei Hua Jin
1Department of Urology and the Urological Science Institute, Yonsei University College of Medicine, Seoul, Korea.
International Neurourology Journal
|July 21, 2012
Summary
Bladder outlet obstruction (BOO) in rats increased transient receptor potential cation channel subfamily M member 8 (TRPM8) expression, potentially contributing to voiding dysfunction. TRPM8 regulation offers a possible avenue for treating overactive bladder (OAB).
Area of Science:
- Urology
- Physiology
- Molecular Biology
Background:
- Bladder outlet obstruction (BOO) is a common cause of lower urinary tract symptoms, including storage and voiding dysfunction.
- Overactive bladder (OAB) is a significant condition characterized by urinary urgency, frequency, and nocturia.
- Transient receptor potential cation channel subfamily M member 8 (TRPM8) is a cold and chemical sensor implicated in various physiological processes.
Purpose of the Study:
- To investigate the expression of TRPM8 in a rat model of BOO.
- To evaluate the relationship between TRPM8 expression and the development of OAB symptoms in BOO.
- To explore the potential therapeutic implications of TRPM8 modulation for OAB.
Main Methods:
- Establishment of a rat model of BOO.
- Cystometry to assess bladder function (intercontraction interval, micturition pressure, threshold pressure).
- Histological analysis (Masson's trichrome staining) and molecular analysis (immunofluorescence, RT-PCR) to quantify TRPM8 expression in bladder tissue and dorsal root ganglia.
Main Results:
- BOO rats exhibited significantly increased micturition pressure and decreased intercontraction interval, indicative of voiding dysfunction.
- Histological examination revealed detrusor muscle hypertrophy and thickened mucosa in BOO bladders.
- TRPM8-positive cells and mRNA levels were significantly elevated in the bladders and dorsal root ganglia of BOO rats compared to controls.
Conclusions:
- Increased bladder wall thickness and collagen proportion in BOO may contribute to voiding dysfunction.
- Elevated TRPM8 expression in BOO suggests a role in Ca(2+) influx and smooth muscle contraction, potentially exacerbating OAB symptoms.
- While menthol treatment did not resolve OAB symptoms despite increased TRPM8 expression, TRPM8 regulation presents a potential therapeutic target for OAB.
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