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BTA is a zinc-dependent endopeptidase, which binds to and is taken up by, neurons via a high-affinity interaction with synaptic vesicle protein 2 (SV2) ( 5). Several serotypes of the toxin are produced, among which type A is the most potent ( 4). Although it is recognized that there are multiple formulations of BTA and that all are not identical in potency and biological availability ( 2), BTA is used as an abbreviation herein to refer to all commercially available forms of BTA.īTA is a neurotoxin produced by the bacteria Clostridium botulinum ( 3). Interestingly, there has also been an increase in descriptions of transport of BTA to the CNS and its activity within the CNS. This review discusses potential mechanisms of action of BTA, locations at which BTA may have an effect, and emerging evidence that chronic PBS/IC may induce plasticity within the central nervous system (CNS) that results in persistence of symptoms. The outcome of treatment of PBS/IC symptoms with BTA has varied, and this may relate to the heterogeneity of causes underlying PBS/IC, plasticity of the nervous system induced by PBS/IC, and disparity of effects of BTA in individual patients. Since that time, BTA has been used to treat a variety of LUT disorders, including painful bladder syndrome/interstitial cystitis (PBS/IC). The therapeutic use of botulinum toxin A (BTA) to treat LUT disorders was first described in 1988 ( 1). Fatal at sufficient doses, the controlled use of botulinum toxin has been demonstrated to be an effective treatment for a variety of disorders, including those of the lower urinary tract (LUT). Botulinum toxin is among the most potent toxins known.