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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

Representative images of SChG-UBPN in BTX-treated pigs. All images were taken separately from blue (a, d, g, j, m), green (b, e, h, k, n) and red (c, f, i, l, o) fluorescent channels. a–c Five FB+ neurons (a, blue, 1 long arrow, 3 short arrows, 1 double arrow), which were simultaneously DβH+ (b, green, 1 long arrow, 3 short arrows) or DβH- (1 double arrow) and NPY+ (c, red, 1 long arrow, 1 double arrow) or NPY- (3 short arrows). d–f Three FB+ neurons (d, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 2 long arrows, 1 short arrow) and VIP+ (f, red, 2 long arrows) or VIP- (1 short arrow). g–i Three FB+ neurons (g, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (h, green, 2 long arrows, 1 short arrow) and SOM+ (i, red, 2 long arrows) or SOM- (1 short arrow). j–l Seven FB+ neurons (j, blue, 5 long arrows, 2 short arrows), which were simultaneously DβH+ (k, green, 5 long arrows, 2 short arrows) and L-ENK+ (l, red, 5 long arrows) or L-ENK- (2 short arrows). m–o Three FB+ neurons (m, blue; 2 long arrows, 1 double arrow), which were simultaneously DβH+ (n, green, 2 long arrows) or DβH- (1 double arrow) and nNOS+ (o, red, 2 long arrows) or nNOS- (1 double arrow). Bars 50 μm (a–f, m–o), 20 μm (g–l)
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Fig4: Representative images of SChG-UBPN in BTX-treated pigs. All images were taken separately from blue (a, d, g, j, m), green (b, e, h, k, n) and red (c, f, i, l, o) fluorescent channels. a–c Five FB+ neurons (a, blue, 1 long arrow, 3 short arrows, 1 double arrow), which were simultaneously DβH+ (b, green, 1 long arrow, 3 short arrows) or DβH- (1 double arrow) and NPY+ (c, red, 1 long arrow, 1 double arrow) or NPY- (3 short arrows). d–f Three FB+ neurons (d, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 2 long arrows, 1 short arrow) and VIP+ (f, red, 2 long arrows) or VIP- (1 short arrow). g–i Three FB+ neurons (g, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (h, green, 2 long arrows, 1 short arrow) and SOM+ (i, red, 2 long arrows) or SOM- (1 short arrow). j–l Seven FB+ neurons (j, blue, 5 long arrows, 2 short arrows), which were simultaneously DβH+ (k, green, 5 long arrows, 2 short arrows) and L-ENK+ (l, red, 5 long arrows) or L-ENK- (2 short arrows). m–o Three FB+ neurons (m, blue; 2 long arrows, 1 double arrow), which were simultaneously DβH+ (n, green, 2 long arrows) or DβH- (1 double arrow) and nNOS+ (o, red, 2 long arrows) or nNOS- (1 double arrow). Bars 50 μm (a–f, m–o), 20 μm (g–l)

Mentions: Double-labelling immunohistochemistry revealed that, similar to the control group, the vast majority of FB+ UBPN (89.8 ± 2.5 % in BTX-treated animals vs 91 ± 2.3 % in the control group) were DβH+ (Fig. 4b, e, h, k, n). The remaining nerve cells (Fig. 4b, n) were also DβH- (10.2 ± 2.5 % in BTX-treated animals vs 9 ± 2.3 % in the control group).Fig. 4


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)

Representative images of SChG-UBPN in BTX-treated pigs. All images were taken separately from blue (a, d, g, j, m), green (b, e, h, k, n) and red (c, f, i, l, o) fluorescent channels. a–c Five FB+ neurons (a, blue, 1 long arrow, 3 short arrows, 1 double arrow), which were simultaneously DβH+ (b, green, 1 long arrow, 3 short arrows) or DβH- (1 double arrow) and NPY+ (c, red, 1 long arrow, 1 double arrow) or NPY- (3 short arrows). d–f Three FB+ neurons (d, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 2 long arrows, 1 short arrow) and VIP+ (f, red, 2 long arrows) or VIP- (1 short arrow). g–i Three FB+ neurons (g, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (h, green, 2 long arrows, 1 short arrow) and SOM+ (i, red, 2 long arrows) or SOM- (1 short arrow). j–l Seven FB+ neurons (j, blue, 5 long arrows, 2 short arrows), which were simultaneously DβH+ (k, green, 5 long arrows, 2 short arrows) and L-ENK+ (l, red, 5 long arrows) or L-ENK- (2 short arrows). m–o Three FB+ neurons (m, blue; 2 long arrows, 1 double arrow), which were simultaneously DβH+ (n, green, 2 long arrows) or DβH- (1 double arrow) and nNOS+ (o, red, 2 long arrows) or nNOS- (1 double arrow). Bars 50 μm (a–f, m–o), 20 μm (g–l)
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Fig4: Representative images of SChG-UBPN in BTX-treated pigs. All images were taken separately from blue (a, d, g, j, m), green (b, e, h, k, n) and red (c, f, i, l, o) fluorescent channels. a–c Five FB+ neurons (a, blue, 1 long arrow, 3 short arrows, 1 double arrow), which were simultaneously DβH+ (b, green, 1 long arrow, 3 short arrows) or DβH- (1 double arrow) and NPY+ (c, red, 1 long arrow, 1 double arrow) or NPY- (3 short arrows). d–f Three FB+ neurons (d, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 2 long arrows, 1 short arrow) and VIP+ (f, red, 2 long arrows) or VIP- (1 short arrow). g–i Three FB+ neurons (g, blue, 2 long arrows, 1 short arrow), which were simultaneously DβH+ (h, green, 2 long arrows, 1 short arrow) and SOM+ (i, red, 2 long arrows) or SOM- (1 short arrow). j–l Seven FB+ neurons (j, blue, 5 long arrows, 2 short arrows), which were simultaneously DβH+ (k, green, 5 long arrows, 2 short arrows) and L-ENK+ (l, red, 5 long arrows) or L-ENK- (2 short arrows). m–o Three FB+ neurons (m, blue; 2 long arrows, 1 double arrow), which were simultaneously DβH+ (n, green, 2 long arrows) or DβH- (1 double arrow) and nNOS+ (o, red, 2 long arrows) or nNOS- (1 double arrow). Bars 50 μm (a–f, m–o), 20 μm (g–l)
Mentions: Double-labelling immunohistochemistry revealed that, similar to the control group, the vast majority of FB+ UBPN (89.8 ± 2.5 % in BTX-treated animals vs 91 ± 2.3 % in the control group) were DβH+ (Fig. 4b, e, h, k, n). The remaining nerve cells (Fig. 4b, n) were also DβH- (10.2 ± 2.5 % in BTX-treated animals vs 9 ± 2.3 % in the control group).Fig. 4

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