Resiniferatoxin (RTX)-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.

authors

Mariusz Majewski, Agnieszka Bossowska, Joanna Wojtkiewicz, Celina Kowalska, Izabela Janiuk, Artur Zapart, Andrzej Borkowski, Piotr Radziszewski

Katedra Fizjologii Człowieka, Wydział Nauk Medycznych, Uniwersytet Warmińsko-Mazurski w Olsztynie
Klinika Urologii Ogólnej, Onkologicznej i Czynnościowej Warszawskiego Uniwersytetu Medycznego

summary

Introduction.

Resiniferatoxin (RTX) is a natural, highly potent neurotoxin acting by activa-tion of the vanilloid receptor in a subpopulation of primary afferent sensory neurons involved in nociception. Although this substance becomes more often used in experimental therapy of sensory system disorders, to the present time there is no data concerning the influence of RTX on the chemical coding of sympathetic IMG neurons supplying the urinary bladder in the pig, an animal species that can be used as a very good animal model for human lower urinary tract.

Objectives.

The present study was aimed at revealing the chemical coding of IMG neurons supplying urinary bladder after intravesical instillation of RTX.

Materials and methods.

Urinary bladder wall was injected with retrograde tracer Fast Blue (FB) in twelve juvenile female pigs and an intravesical instillation of RTX (500 nmol per animal) was performed three weeks later in six of them. One week later, IMGs were collected from all animals and were processed for a routine single- and double-immunofluorescence labeling on 10 μm-thick cryostat sections.

Results.

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), vasoative intestinal polypeptide (VIP), calbidin (CB) and galanin (GAL; 2.2%; 2%; 1.7% and 1.2%, respectively). After RTX-treatment, a significant decrease in the number of FB+ neurons containing NPY and VIP were observed (55%, 0), while the number of SOM and GAL-IR bladder-projecting sympathetic neurons increased (up to 55% and 13%, respectively). Changes in the “solely” noradrenergic neurons (TH/DβH-IR) were not observed.

Conclusions.

As may be judged from the results of the present study, RTX appears to be able to induce changes in the chemical coding of not only sensory neurons, but also of noradrenergic cells constituting the efferent limb of the filling phase. Thus, it appears that in further studies focusing on the RTX usage in the therapy of neurogenic bladder illnesses, this neurotoxin may also be possibly applied in the cases of disturbed neural control of the detrusor; however, this hypothesis must be further experimentally validated.