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CCDC, a G-protein coupled receptor, is found mainly on enteroendocrine cells where it is thought to be involved in cell survival and proliferation and regulation of innate immunity and glucose metabolism¹⁴. Here, we have shown that the murine homologue of human TGR5 is found at high levels on bladder afferent neurons where it can mediate mechanical sensitisation in response to bladder distension. We found that activation of TGR5 by CCDC in vitro increased afferent firing in a dose-dependent manner in responses to both distension and spontaneous activity, effects mediated by a NO-dependent pathway, TRPV1 and K_Ca^{²⁺ channels, activation of MAP kinase ERK, and increased BKCa channels. TRPV1 agonists capsaicin, allyl isothiocyanate and Pg5 and the synthetic TGR5 agonist CCDC induce [Ca²⁺]_i transients in DRG neurons in vitro that are comparable to those observed in vivo following CCDC administration. Importantly, we found that pharmacological activation of TGR5 causes hypersensitivity to bladder distension ex vivo and that these effects are abolished in Tgr5^/ mice.}

The overlapping symptoms of OAB and IC/BPS, including frequency, urgency and discomfort indicate an increase in the sensitivity of bladder afferent neurons to bladder filling. Identifying the receptors and channels involved in bladder afferent neuronal activation, and the impact these have on behavioural responses in states of health and hypersensitivity, is a crucial step to developing efficacious treatment options for patients suffering bladder hypersensitivity disorders. Here, we have identified a role for the bile acid receptor TGR5 in mediating bladder afferent mechanical hypersensitivity in vivo and ex vivo. Intravesical administration of the progesterone metabolite Pg5 and the synthetic TGR5 agonist CCDC increased afferent sensitivity to bladder distension at both peripheral and spinal levels, responses which we show to be reduced or absent in mice lacking the gene for TGR5 (Gpbar1).

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