ArticleNeurochemistry international2008
Botulinum toxin type A normalizes alterations in urothelial ATP and NO release induced by chronic spinal cord injury.
Article in Neurochemistry international, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 116 citations in OpenAlex.
- Intravesical instillation of botulinum toxin A: an in vivo murine study and pilot clinical trial.International urology and nephrology · 2011Trial
- Acute Chemodenervation of the Bladder With Botulinum Toxin After Spinal Cord Injury Resulted in Preserved Bladder Function in Rodents.Neurourology and urodynamics · 2025Article
- Mechanisms of oxidative stress in interstitial cystitis/bladder pain syndrome.Nature reviews. Urology · 2024Review
- Targeting neurotrophin and nitric oxide signaling to promote recovery and ameliorate neurogenic bladder dysfunction following spinal cord injury - Mechanistic concepts and clinical implications.Continence (Amsterdam, Netherlands) · 2023Article
- Molecular Mechanisms of Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury.International journal of molecular sciences · 2023Review
- Review
- Review
- Article
- Urinary adenosine triphosphate and nitric oxide levels in patients with underactive bladder: a preliminary study.World journal of urology · 2021Article
- Purinergic signalling in the urinary bladder - When function becomes dysfunction.Autonomic neuroscience : basic & clinical · 2021Article
- Overactive Bladder Symptoms Within Nervous System: A Focus on Etiology.Frontiers in physiology · 2021Review
- Frontiers in the Clinical Applications of Botulinum Toxin A as Treatment for Neurogenic Lower Urinary Tract Dysfunction.International neurourology journal · 2020Article
- Article
- Review
- Recommendations for evaluation of bladder and bowel function in pre-clinical spinal cord injury research.The journal of spinal cord medicine · 2020Review
- Mechanism of Action of Botulinum Toxin A in Treatment of Functional Urological Disorders.Toxins · 2020Review
- Review
- Clinical application of intravesical botulinum toxin type A for overactive bladder and interstitial cystitis.Investigative and clinical urology · 2020Review
- Purinergic receptor mediated calcium signalling in urothelial cells.Scientific reports · 2019Article
- The Botulinum Treatment of Neurogenic Detrusor Overactivity: The Double-Face of the Neurotoxin.Toxins · 2019Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
The purpose of this paper was to simultaneously examine changes in urothelial ATP and NO release in normal and spinal cord injured animals as well as in spinal cord injured animals treated with botulinum toxin type A (BoNT-A). Furthermore we correlated changes in transmitter release with functional changes in bladder contraction frequency, and determined the effects of BoNT-A on bladder efferent nerve function. Normal and spinal cord injured rat bladders were injected on day 0 with either vehicle (saline containing bovine serum albumin) or BoNT-A. On day 2, in vitro neurotransmitter release and bladder strip contractility studies as well as in vivo cystometrographic studies were conducted. Resting ATP release was significantly enhanced following spinal cord injury (i.e. 57% increase, p<0.05) and was unaffected by BoNT-A treatment. SCI increased hypoosmotic evoked urothelial ATP release by 377% (p<0.05). BoNT-A treatment reduced evoked ATP release in SCI bladders by 83% (p<0.05). In contrast, hypoosmotic stimulation induced NO release was significantly inhibited following SCI (i.e. 50%, p<0.05) but recovered in SCI rats treated with BoNT-A (i.e. 195% increase in NO release in SCI-BTX-treated rats compared to SCI controls, p<0.01). Changes in urothelial transmitter release coincided with a significant decrease in non-voiding bladder contraction frequency (i.e. 71%, p<0.05) in SCI-BTX rats compared to SCI rats. While no difference was measured between neurally evoked contractile amplitude between SCI and SCI-BTX animals, atropine (1 microM) inhibited contractile amplitude to a greater extent (i.e. 76%, p<0.05) in the SCI-BTX group compared to the SCI group. We hypothesize that alterations in the ratio of excitatory (i.e. ATP) and inhibitory (i.e. NO) urothelial transmitters promote bladder hyperactivity in rat bladders following SCI that can be reversed, to a large extent, by treatment with BoNT-A.
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