PTU - Polskie Towarzystwo Urologiczne
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Botulinum toxin (BTX)-induced changes in the chemical coding of inferior mesenteric ganglion (IMG) neurons supplying porcine urinary bladder
Article published in Urologia Polska 2008/61/Supl. 1.


Joanna Wojtkiewicz, Agnieszka Bossowska, Artur Zapart, Cezary Skobowiat, Izabela Janiuk, Andrzej Borkowski, Piotr Radziszewski, Mariusz Majewski
Katedra Fizjologii Człowieka, Wydział Nauk Medycznych, Uniwersytet Warmińsko-Mazurski w Olsztynie
Klinika Urologii Ogólnej, Onkologicznej i Czynnościowej Warszawskiego Uniwersytetu Medycznego



Botulinum toxin of the A type (BTX), one of the most powerful neurotoxins known so far, becomes one of the most effective drug in the experimental therapy of a range of neurogenic urinary bladder disorders. Although as of now its mode of action on the cholinergic component of the bladder innervation is relatively well-known, there is still a lack of data concerning possible action of this neurotoxin on other components of the peripheral nervous system controlling the functions of the bladder.


The present study was aimed at revealing the chemical coding of IMG neurons supplying urinary bladder of the pig (used here as an animal model of the human organ), after intravesical BTX injections.

Materials and methods.

Urinary bladder wall was injected with retrograde tracer Fast Blue (FB) in twelve juvenile female pigs and three weeks later six of them were injected with botulinum toxin A by aid of a cystoscope (100 IU per animals, Botox). One week later, IMGs were collected from all animals and processed for a routine doubleimmunofluorescence labeling on 10 μm cryostat sections.


In control animals, the vast majority of FB+ neurons contained tyrosine hydroxylase/ dopamine β-hydroxylase (TH/DβH) and/or neuropeptide Y(NPY-IR (95% and 85% of all retrogradely labeled neurons, respectively). A small number of FB+ cells contained also somatostatin (SOM), vasoactive intestinal polypeptide (VIP), calbindin (CB) and galanin (GAL; 2.2%; 2%; 1.7% and 1.2%, respectively). One week after BTX injections into the bladder wall, a significant decrease in the number of FB+ neurons
containing TH/DβH, NPY and VIP was observed (till 85%, 29% and 0%, respectively), while the numbers of SOM- and CB-IR sympathetic neurons increased (up to 18% and 12%, respectively).


As may be judged from the results obtained in the present study, BTX is able to modify not only the chemical phenotypes of cholinergic or sensory neurons, but also influence the kind of neurotransmitter substances synthesized by sensory neurons. Thus, it appears possible, that this neurotoxin may eventually be used in the therapy of the overactive sympathetic component of the urinary bladder innervation. However, this suggestion must be verified by further studies.