Fiber type-specific afferent nerve activity induced by transient contractions of rat bladder smooth muscle in pathological states.

Nahoko Kuga,Asao Tanioka,Tomoyuki Kawai,Koichiro Hagihara,Gennady Cymbalyuk

doi:10.1371/journal.pone.0189941

Abstract

Bladder smooth muscle shows spontaneous phasic contractions, which undergo a variety of abnormal changes depending on pathological conditions. How abnormal contractions affect the activity of bladder afferent nerves remains to be fully tested. In this study, we examined the relationship between transient increases in bladder pressure, representing transient contraction of bladder smooth muscle, and spiking patterns of bladder afferent fibers of the L6 dorsal root, in rat pathological models. All recordings were performed at a bladder pressure of approximately 10 cmH2O by maintaining the degree of bladder filling. In the cyclophosphamide-induced model, both Aδ and C fibers showed increased sensitivity to transient bladder pressure increases. In the prostaglandin E2-induced model, Aδ fibers, but not C fibers, specifically showed overexcitation that was time-locked with transient bladder pressure increases. These fiber type-specific changes in nerve spike patterns may underlie the symptoms of urinary bladder diseases.

Highlights

Bladder smooth muscle shows spontaneous transient contractions
We first monitored how the transient bladder pressure (BP) increases were altered in the two animal models: (i) the CYPinduced model and (ii) the prostaglandin E2 (PGE2)-induced model
In C fibers no marked increase in the proportion of synchronized fibers was detected in the presence of PGE2 and the average frequency ratio remained unchanged (Fig 3C). These results suggest that Aδ fibers are able to sense transient BP increases in PGE2-induced overactive bladders, whereas C fibers are insensitive

Summary

Introduction

It has been shown that there are pronounced abnormal changes in the patterns of transient contractions in both human patients [1, 2] and animal disease models, including the cyclophosphamide (CYP)induced cystitis [3, 4] animal model and animal models with detrusor overactivity induced by prostaglandin E2 (PGE2). While early studies have reported the relationship between pathological contractions and bladder nerve activity [9,10,11,12,13], detailed characteristics of the physiological dynamics have not been fully elucidated

Results

Discussion

Conclusion