Related Experiment Video
Updated: May 22, 2026
09:39
Establishing a Mouse Model of a Pure Small Fiber Neuropathy with the Ultrapotent Agonist of Transient Receptor Potential Vanilloid Type 1
Published on: February 13, 2018
Transient receptor potential vanilloid 1 mediates nerve growth factor-induced bladder hyperactivity and noxious input
Barbara Frias1, Ana Charrua, Antonio Avelino
1Department of Experimental Biology, Faculty of Medicine, University of Porto, Porto, Portugal.
BJU International
|May 1, 2012
Summary
Nerve growth factor (NGF) causes bladder overactivity by interacting with TRPV1 channels. Blocking TRPV1 prevents NGF-induced bladder dysfunction, highlighting TRPV1 as a therapeutic target for bladder pathologies.
Area of Science:
- Urology
- Neuroscience
- Pharmacology
Background:
- Nerve growth factor (NGF) plays a role in sensory processing and can influence bladder function.
- Transient receptor potential vanilloid 1 (TRPV1) is a key receptor involved in pain and sensory signaling.
- Dysregulation of bladder sensory input can lead to various bladder dysfunctions.
Purpose of the Study:
- To investigate the role of TRPV1 in NGF-induced bladder sensory changes and reflex activity.
- To determine if TRPV1 is a potential therapeutic target for NGF-associated bladder dysfunction.
Main Methods:
- Wild-type and TRPV1 knockout mice received NGF or saline injections for 4 days.
- Thermal sensitivity, cystometry (measuring bladder reflex contractions), and spinal c-Fos expression were assessed.
- TrkA receptor expression was analyzed in spinal cord and dorsal root ganglia.
Main Results:
- NGF induced thermal hypersensitivity in wild-type mice but not in TRPV1 knockout mice.
- NGF significantly increased bladder reflex contraction frequency and AUC in wild-type mice, an effect absent in TRPV1 knockout mice.
- NGF increased spinal c-Fos expression in wild-type mice, indicating heightened sensory input, which was not observed in TRPV1 knockout mice.
Conclusions:
- NGF-induced bladder overactivity and sensory dysfunction are dependent on TRPV1.
- The absence of bladder overactivity in TRPV1 knockout mice treated with NGF is not due to altered TrkA expression.
- TRPV1 is crucial for NGF-driven bladder dysfunction, making it a promising therapeutic target for conditions involving NGF upregulation.
Related Concept Videos
01:30Ligand-Gated Ion Channel Receptor: Gating Mechanism
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
01:12Mechanically-gated Ion Channels
Mechanically-gated ion channels are proteins found in eukaryotic and prokaryotic cell membranes that open in response to mechanical stress. Tension, compression, swelling, and shear stress can alter the conformation of the protein, opening a transmembrane channel that allows the passage of ions for signal transmission. In eukaryotes, mechanically-gated channels are distributed in several regions like the neurons, lungs, skin, bladder, and heart, where they play critical roles in numerous...