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Phasic, Rapidly‐Propagating Calcium Transients Occur in a Non‐Muscle Cell Network within the Mouse Urinary Bladder Wall
Author(s) -
Tykocki Nathan R.,
Hennig Grant W.,
Koide Masayo,
Wellman George C,
Nelson Mark T.
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.837.5
Subject(s) - trpv1 , detrusor muscle , transient receptor potential channel , urinary bladder , urothelial cell , chemistry , myocyte , capsaicin , overactive bladder , anatomy , microbiology and biotechnology , biophysics , medicine , biology , urothelium , receptor , pathology , biochemistry , alternative medicine
Multiple species, including humans, exhibit “non‐voiding” or “transient” contractions of the bladder wall during filling that are accompanied by large bursts of activity from bladder sensory nerves. This suggests that transient contractions play an important role as sensors of bladder fullness, but how transient contractions are generated remains unclear. Using genetically‐encoded Ca 2+ indicator mice and novel macroscopic imaging techniques, we sought to determine what Ca 2+ signals drive TC generation and coordination across the bladder wall. We utilized mice that constitutively express the Ca 2+ indicators GCaMP5 or GCaMP6f as an expression‐dependent fate map of smooth muscle cells ( Acta2 promoter) or non‐muscle cells ( Trpv1 promoter) within the urinary bladder wall. We discovered that transient pressure events (TPEs) are actually the integration of numerous micro‐contractions of the bladder wall. These micromotions vary in position, frequency and duration, but result in regular, phasic increases in intravesical pressure. Ca 2+ events in urinary bladder smooth muscle (UBSM) were restricted to small patches muscle cells and seemed to occur stochastically. Interestingly, we discovered a network of cells within the bladder wall of Trpv1‐ GCaMP6f mice that were neither smooth muscle cells nor nerve fibers. This network exhibited extremely rapid and phasic Ca 2+ transients that propagated quickly across the entire bladder wall, suggesting that the cells were electrically coupled. The slower waxing and waning of the high‐frequency Ca 2+ transient intensity closely aligned with the frequency of TPEs. Surprisingly, this network of cells was unresponsive to the TRPV1 agonist capsaicin, suggesting that TRPV1 channels were no longer functional in these cells. These data suggest that the bladder wall micro‐motions underlying TPEs may be driven by phasic Ca 2+ transients that occur in a non‐muscle cell network within the bladder wall. Support or Funding Information Supported by NIH K01DK103840 (NRT) and R37DK053832 (MTN). This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .