BoNT/A in the Urinary Bladder—More to the Story than Silencing of Cholinergic Nerves |
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| Authors: | Hodan Ibrahim Jacquie Maignel Fraser Hornby Donna Daly Matthew Beard |
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| Affiliation: | 1.Department of Pharmacy and Biomedical Science, University of Central Lancashire, Preston PR1 2HE, UK; (H.I.); (D.D.);2.Ipsen Innovation, 5 Avenue du Canada, 91940 Les Ulis, France;3.Ipsen Bioinnovation, 102 Park Drive, Milton Park, Abingdon OX14 4RY, UK; |
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| Abstract: | ![]()
Botulinum neurotoxin (BoNT/A) is an FDA and NICE approved second-line treatment for overactive bladder (OAB) in patients either not responsive or intolerant to anti-cholinergic drugs. BoNT/A acts to weaken muscle contraction by blocking release of the neurotransmitter acetyl choline (ACh) at neuromuscular junctions. However, this biological activity does not easily explain all the observed effects in clinical and non-clinical studies. There are also conflicting reports of expression of the BoNT/A protein receptor, SV2, and intracellular target protein, SNAP-25, in the urothelium and bladder. This review presents the current evidence of BoNT/A’s effect on bladder sensation, potential mechanisms by which it might exert these effects and discusses recent advances in understanding the action of BoNT in bladder tissue. |
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| Keywords: | botulinum neurotoxin neurotoxin bladder urology urothelium SNAP-25 SV2 |
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