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Changes in chemical coding of sympathetic chain ganglia (SChG) neurons supplying porcine urinary bladder after botulinum toxin (BTX) treatment.

Lepiarczyk E, Bossowska A, Majewski M - Cell Tissue Res. (2015)

Bottom Line: Botulinum toxin (BTX) is a neurotoxin used in medicine as an effective drug in experimental therapy of neurogenic urinary bladder disorders.BTX injections caused a decrease in the number of FB+/DβH+ neurons that were immunopositive to NPY (39.5 ± 4.5 % vs 74.5 ± 11.9 %), VIP (8.9 ± 5.3 % vs 22.3 ± 8.8 %), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) and a distinct increase in the number of FB+/DβH+ neurons that were immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 % ± 0.8 %) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %).Our study provides novel evidence that the therapeutic effects of BTX on the mammalian urinary bladder are partly mediated by SChG neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Physiology, Faculty of Medical Sciences, University of Warmia and Mazury in Olsztyn, Warszawska 30, 10-082, Olsztyn, Poland, ewa.lepiarczyk@uwm.edu.pl.

ABSTRACT
Botulinum toxin (BTX) is a neurotoxin used in medicine as an effective drug in experimental therapy of neurogenic urinary bladder disorders. We have investigated the influence of BTX on the chemical coding of sympathetic chain ganglia (SChG) neurons supplying the porcine urinary bladder. The toxin was injected into the wall of the bladder. SChG neurons were visualized by a retrograde tracing method with fluorescent tracer fast blue (FB) and their chemical coding was investigated by double-labelling immunohistochemistry with antibodies against dopamine β-hydroxylase (DβH; a marker of noradrenergic neurons), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), somatostatin (SOM), galanin (GAL), Leu(5)-enkephalin (L-ENK) and neuronal nitric oxide synthase (nNOS). In both the control (n = 5) and BTX-treated pigs (n = 5), the vast majority (91 ± 2.3 % and 89.8 ± 2.5 %, respectively) of FB-positive (FB+) nerve cells were DβH+. BTX injections caused a decrease in the number of FB+/DβH+ neurons that were immunopositive to NPY (39.5 ± 4.5 % vs 74.5 ± 11.9 %), VIP (8.9 ± 5.3 % vs 22.3 ± 8.8 %), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) and a distinct increase in the number of FB+/DβH+ neurons that were immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 % ± 0.8 %) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %). Our study provides novel evidence that the therapeutic effects of BTX on the mammalian urinary bladder are partly mediated by SChG neurons.

No MeSH data available.


Related in: MedlinePlus

Bar diagram showing relative frequencies (%) of subpopulations of noradrenergic (DβH+) retrogradely labelled (FB+) bladder-projecting neurons in sympathetic chain ganglia (SChG) of control pigs (n = 5, open bars) and BTX-treated animals (n = 5, solid bars). Each bar represents mean ± SD of pooled data from bilateral L3, L5 and S2 SChG (DβH dopamine β-hydroxylase, NPY neuropeptide Y, VIP vasoactive intestinal polypeptide, SOM somatostatin, GAL galanin, L-ENK Leu5-enkephalin, nNOS neuronal nitric oxide synthase). Statistically significant differences: **P ≤ 0.01, ***P ≤ 0.005
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Fig5: Bar diagram showing relative frequencies (%) of subpopulations of noradrenergic (DβH+) retrogradely labelled (FB+) bladder-projecting neurons in sympathetic chain ganglia (SChG) of control pigs (n = 5, open bars) and BTX-treated animals (n = 5, solid bars). Each bar represents mean ± SD of pooled data from bilateral L3, L5 and S2 SChG (DβH dopamine β-hydroxylase, NPY neuropeptide Y, VIP vasoactive intestinal polypeptide, SOM somatostatin, GAL galanin, L-ENK Leu5-enkephalin, nNOS neuronal nitric oxide synthase). Statistically significant differences: **P ≤ 0.01, ***P ≤ 0.005

Mentions: However, in BTX-treated pigs, the percentages of FB+ noradrenergic neuronal subpopulations distinctly varied from those determined in the control animals (Fig. 5). A lower number of FB+/DβH+/NPY+ neurons (39.5 ± 4.5 % vs 74.5 ± 11.9 %) were observed in BTX-treated pigs (Fig. 4a–c). Furthermore, in the toxin-injected animals a decrease in the number of FB+/DβH+ neurons immunopositive to VIP (8.9 ± 5.3 % vs 22.3 % ± 8.8 %; Fig. 4d–f), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %; Fig. 4g–i) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) was observed. On the other hand, in BTX-injected pigs, an increase in the number of the noradrenergic UBPN immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 ± 0.8 %; Fig. 4j–l) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %; Fig. 4m–o) was observed.Fig. 5


Changes in chemical coding of sympathetic chain ganglia (SChG) neurons supplying porcine urinary bladder after botulinum toxin (BTX) treatment.

Lepiarczyk E, Bossowska A, Majewski M - Cell Tissue Res. (2015)

Bar diagram showing relative frequencies (%) of subpopulations of noradrenergic (DβH+) retrogradely labelled (FB+) bladder-projecting neurons in sympathetic chain ganglia (SChG) of control pigs (n = 5, open bars) and BTX-treated animals (n = 5, solid bars). Each bar represents mean ± SD of pooled data from bilateral L3, L5 and S2 SChG (DβH dopamine β-hydroxylase, NPY neuropeptide Y, VIP vasoactive intestinal polypeptide, SOM somatostatin, GAL galanin, L-ENK Leu5-enkephalin, nNOS neuronal nitric oxide synthase). Statistically significant differences: **P ≤ 0.01, ***P ≤ 0.005
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Related In: Results  -  Collection

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Fig5: Bar diagram showing relative frequencies (%) of subpopulations of noradrenergic (DβH+) retrogradely labelled (FB+) bladder-projecting neurons in sympathetic chain ganglia (SChG) of control pigs (n = 5, open bars) and BTX-treated animals (n = 5, solid bars). Each bar represents mean ± SD of pooled data from bilateral L3, L5 and S2 SChG (DβH dopamine β-hydroxylase, NPY neuropeptide Y, VIP vasoactive intestinal polypeptide, SOM somatostatin, GAL galanin, L-ENK Leu5-enkephalin, nNOS neuronal nitric oxide synthase). Statistically significant differences: **P ≤ 0.01, ***P ≤ 0.005
Mentions: However, in BTX-treated pigs, the percentages of FB+ noradrenergic neuronal subpopulations distinctly varied from those determined in the control animals (Fig. 5). A lower number of FB+/DβH+/NPY+ neurons (39.5 ± 4.5 % vs 74.5 ± 11.9 %) were observed in BTX-treated pigs (Fig. 4a–c). Furthermore, in the toxin-injected animals a decrease in the number of FB+/DβH+ neurons immunopositive to VIP (8.9 ± 5.3 % vs 22.3 % ± 8.8 %; Fig. 4d–f), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %; Fig. 4g–i) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) was observed. On the other hand, in BTX-injected pigs, an increase in the number of the noradrenergic UBPN immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 ± 0.8 %; Fig. 4j–l) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %; Fig. 4m–o) was observed.Fig. 5

Bottom Line: Botulinum toxin (BTX) is a neurotoxin used in medicine as an effective drug in experimental therapy of neurogenic urinary bladder disorders.BTX injections caused a decrease in the number of FB+/DβH+ neurons that were immunopositive to NPY (39.5 ± 4.5 % vs 74.5 ± 11.9 %), VIP (8.9 ± 5.3 % vs 22.3 ± 8.8 %), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) and a distinct increase in the number of FB+/DβH+ neurons that were immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 % ± 0.8 %) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %).Our study provides novel evidence that the therapeutic effects of BTX on the mammalian urinary bladder are partly mediated by SChG neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Physiology, Faculty of Medical Sciences, University of Warmia and Mazury in Olsztyn, Warszawska 30, 10-082, Olsztyn, Poland, ewa.lepiarczyk@uwm.edu.pl.

ABSTRACT
Botulinum toxin (BTX) is a neurotoxin used in medicine as an effective drug in experimental therapy of neurogenic urinary bladder disorders. We have investigated the influence of BTX on the chemical coding of sympathetic chain ganglia (SChG) neurons supplying the porcine urinary bladder. The toxin was injected into the wall of the bladder. SChG neurons were visualized by a retrograde tracing method with fluorescent tracer fast blue (FB) and their chemical coding was investigated by double-labelling immunohistochemistry with antibodies against dopamine β-hydroxylase (DβH; a marker of noradrenergic neurons), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), somatostatin (SOM), galanin (GAL), Leu(5)-enkephalin (L-ENK) and neuronal nitric oxide synthase (nNOS). In both the control (n = 5) and BTX-treated pigs (n = 5), the vast majority (91 ± 2.3 % and 89.8 ± 2.5 %, respectively) of FB-positive (FB+) nerve cells were DβH+. BTX injections caused a decrease in the number of FB+/DβH+ neurons that were immunopositive to NPY (39.5 ± 4.5 % vs 74.5 ± 11.9 %), VIP (8.9 ± 5.3 % vs 22.3 ± 8.8 %), SOM (5.8 ± 2.3 % vs 17.4 ± 3.7 %) or GAL (0.9 ± 1.2 % vs 5.4 ± 4.4 %) and a distinct increase in the number of FB+/DβH+ neurons that were immunoreactive to L-ENK (3.7 ± 2.9 % vs 1.1 % ± 0.8 %) or nNOS (7.7 ± 3.5 % vs 0.8 ± 0.6 %). Our study provides novel evidence that the therapeutic effects of BTX on the mammalian urinary bladder are partly mediated by SChG neurons.

No MeSH data available.


Related in: MedlinePlus