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The TRPV3 ion channel role in regulation of bladder function and sensory nerve activity in a mouse.
Michael A. Maccini, MD, Benjamin J. King, MD, Katarína Zvarová, MD, PhD, Travis K. Mann-Gow, BS, Joseph Yared, MD, Peter Zvara, MD, PhD.
University of Vermont, Burlington, VT, USA.

BACKGROUND: Transient receptor potential vanilloid type 3 (TRPV3) cation channels have been shown to play a role in pain sensation and smooth muscle relaxation. We have previously documented the expression of the TRPV3 channel in the mouse bladder and showed that carvacrol, a component of oregano shown to affect both TRPA1 and TRPV3 cation channels, attenuates acetic acid (AA)-induced detrusor overactivity in vivo. This study aims to elucidate the effect of TRPV3 on bladder sensation.
METHODS: Immunohistochemistry was used to evaluate TRPV3 in dorsal root ganglia (DRG). The contractile response of bladder wall strips was measured following the administration of capsaicin in the presence of a TRPA1 antagonist. Multifiber afferent nerve activity and cystometry were recorded in awake mice during bladder filling and micturition. The intravesical pressure and nerve activity were correlated during bladder filling with 0.9% NaCl, then 0.25% AA in normal saline, followed by carvacrol.
RESULTS: The TRPV3-positive neurons were identified in the L6 and S1 DRG. Carvacrol eliminated the capsaicin-induced phasic contractions of the bladder strips (n=5). This effect was not affected by the TRPA1 antagonist. A 76% increase in the average sensory nerve activity recorded from the postganglionic bladder nerve following AA infusion was reduced 2.8 fold with carvacrol. AA-induced increase in micturition frequency was reverted with carvacrol but no statistically significant change in intravesical pressure was noted (n=5).
CONCLUSIONS: This study demonstrates that carvacrol suppresses sensory signalling and bladder overactivity during AA-induced bladder irritation and this effect is likely mediated through the TRPV3 cation channel.


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