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Effect of Onabotulinum Toxin A on Substance P and Receptor Neurokinin 1 in the Rat Ventral Prostate

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Date 2016 May 5
PMID 27144785
Citations 1
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Abstract

Introduction: The objective of this work is to examine if sensory innervation impacts lower urinary tract symptoms (LUTS). Onabotulinum toxin A (BoNTA) has been used for the treatment of overactive and neurogenic bladder and as a treatment for LUTS secondary to benign prostatic hyperplasia (BPH). The mechanism of how BoNTA impacts LUTS/BPH is unclear. In rats, BoNTA injection causes prostate denervation, apoptosis and atrophy. In clinical trials reduced prostate size and LUTS are observed inconsistently, suggesting a neurologic component. We will examine if BoNTA treatment inhibits substance P production in sensory nerve fibers in the rat prostate.

Methods: Twenty Sprague Dawley rats were divided into four groups including 1X PBS (control, n=6), 2.5 units Onabotulinum toxin A (BoNTA, n=6), 5 units BoNTA (n=6) injected into both lobes of the ventral prostate (VP) and sham surgery (n=2). Rats were Euthanized after one week. Substance P and its receptor neurokinin 1 localization and quantification were performed by counting the number of stained neurons and nerve bundles, by semi-quantitative immunohistochemical analysis and by western analysis.

Results: Substance P was localized in neuronal axons and bundles in the stroma of the VP but not in the epithelium. Receptor neurokinin 1 was identified in neuronal bundles of the stroma and in columnar epithelium of the VP ducts. Substance P decreased ~90% after BoNTA treatment (p=0.0001) while receptor neurokinin 1 did not change by IHC (p=0.213) or Western (p=0.3675).

Conclusions: BoNTA treatment decreases substance P in the rat VP.

Citing Articles

A Comparison of Effectiveness of Thai Traditional Massage and Tamsulosin in Lower Urinary Tract Symptoms: A Randomized Controlled Trial.

Sinsomboon O, Noppakulsatit P, Tassanarong A, Tungsukruthai P, Sriyakul K J Evid Based Integr Med. 2022; 27:2515690X211068825.

PMID: 35001668 PMC: 8753073. DOI: 10.1177/2515690X211068825.

References
1.
McVary K . BPH: epidemiology and comorbidities. Am J Manag Care. 2006; 12(5 Suppl):S122-8. View

2.
Maria G, Brisinda G, Civello I, Bentivoglio A, Sganga G, Albanese A . Relief by botulinum toxin of voiding dysfunction due to benign prostatic hyperplasia: results of a randomized, placebo-controlled study. Urology. 2003; 62(2):259-64; discussion 264-5. DOI: 10.1016/s0090-4295(03)00477-1. View

3.
Walden P, Marinese D, Srinivasan D, Tzoumaka E, Syyong H, Ford A . Effect of neurokinins on canine prostate cell physiology. Prostate. 2004; 63(4):358-68. DOI: 10.1002/pros.20195. View

4.
Silva J, Pinto R, Carvallho T, Coelho A, Avelino A, Dinis P . Mechanisms of prostate atrophy after glandular botulinum neurotoxin type a injection: an experimental study in the rat. Eur Urol. 2008; 56(1):134-40. DOI: 10.1016/j.eururo.2008.07.003. View

5.
Auffenberg G, Helfand B, McVary K . Established medical therapy for benign prostatic hyperplasia. Urol Clin North Am. 2009; 36(4):443-59, v-vi. DOI: 10.1016/j.ucl.2009.07.004. View