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Published on: April 27, 2014
Bladder Trigone as a Sensory Hub: A Narrative Review
Takuya Sadahira1,2, Yuki Maruyama1, Yosuke Mitsui1
1Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, JPN.
The bladder trigone is a key sensory area in the lower urinary tract. Understanding its specialized nerve pathways is crucial for treating bladder dysfunction and pain.
Area of Science:
- Neuroscience
- Urology
- Cell Biology
Background:
- The bladder trigone, a distinct lower urinary tract region, possesses unique sensory innervation.
- Dysregulation of trigonal signaling contributes to lower urinary tract symptoms (LUTS) like urgency and pain.
- The precise structural and functional basis of trigonal sensory signaling remains incompletely understood.
Purpose of the Study:
- To synthesize current evidence on trigonal afferent organization and sensory signaling.
- To integrate anatomical, molecular, and functional data on trigonal sensory pathways.
- To provide a comprehensive perspective on the trigone's role in bladder sensation and dysfunction.
Main Methods:
- Review of anatomical mapping, receptor profiling, and electrophysiological characterization.
- Integration of data on mechanotransduction, purinergic, peptidergic, and TRP signaling.
- Analysis of translational research and functional assays in aging, inflammation, and disease models.
Main Results:
- Identified three principal afferent classes in the trigone with specific molecular markers (P2X3, TRPV1, CGRP, SP, PIEZO1/2, ASICs).
- Observed high expression of PIEZO2, P2RX3, and Nav1.8 in trigeminal dorsal root ganglion neurons.
- Demonstrated that aging, inflammation, and neurotrophic factors drive afferent plasticity underlying abnormal bladder sensation.
Conclusions:
- The bladder trigone acts as a critical sensory hub integrating neuronal, urothelial, and immune signals.
- Understanding trigonal specialization can inform targeted therapies for sensory urgency and bladder dysfunction.
- Early clinical trials with P2X3 antagonists and TRPV1 inhibitors show promise for symptomatic relief.
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