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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 control 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 Seven fast blue-positive (FB+) neurons (a, blue, 5 long arrows, 1 short arrow, 1 double arrow), which were simultaneously DβH+ (b, green, 5 long arrows, 1 short arrow) or DβH- (1double arrow) and NPY+ (c, red, 5 long arrows, 1 double arrow) or NPY- (1 short arrow). d–f Five FB+ neurons (d, blue, 4 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 4 long arrows, 1 short arrow) and VIP+ (f, red, 4 long arrows) or VIP- (1 short arrow). g–i Four FB+ neurons (g, blue, 1 long arrow, 2 short arrows, 1 double arrow), which were simultaneously DβH+ (h, green, 1 long arrow, 2 short arrows) or DβH- (1 double arrow) and SOM+ ( i, red, 1 long arrow, 1 double arrow) or SOM- (2 short arrows). j–l Three FB+ neurons (j, blue, 3 long arrows), which were simultaneously DβH+ (k, green, 3 long arrows) and L-ENK+ (l, red, 3 long arrows). m–o Four FB+ neurons (m, blue, 1 long arrow, 3 short arrows), which were simultaneously DβH+ (n, green, 1 long arrow, 3 short arrows) and nNOS+ (o, red, 1 long arrow) or nNOS- (3 short arrows). Bars 50 μm (a–f), 20 μm (g–o)
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Fig3: Representative images of SChG-UBPN in control 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 Seven fast blue-positive (FB+) neurons (a, blue, 5 long arrows, 1 short arrow, 1 double arrow), which were simultaneously DβH+ (b, green, 5 long arrows, 1 short arrow) or DβH- (1double arrow) and NPY+ (c, red, 5 long arrows, 1 double arrow) or NPY- (1 short arrow). d–f Five FB+ neurons (d, blue, 4 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 4 long arrows, 1 short arrow) and VIP+ (f, red, 4 long arrows) or VIP- (1 short arrow). g–i Four FB+ neurons (g, blue, 1 long arrow, 2 short arrows, 1 double arrow), which were simultaneously DβH+ (h, green, 1 long arrow, 2 short arrows) or DβH- (1 double arrow) and SOM+ ( i, red, 1 long arrow, 1 double arrow) or SOM- (2 short arrows). j–l Three FB+ neurons (j, blue, 3 long arrows), which were simultaneously DβH+ (k, green, 3 long arrows) and L-ENK+ (l, red, 3 long arrows). m–o Four FB+ neurons (m, blue, 1 long arrow, 3 short arrows), which were simultaneously DβH+ (n, green, 1 long arrow, 3 short arrows) and nNOS+ (o, red, 1 long arrow) or nNOS- (3 short arrows). Bars 50 μm (a–f), 20 μm (g–o)

Mentions: Double-labelling immunohistochemistry revealed two main populations of FB+ neurons. The vast majority (91 ± 2.3 %) of the retrogradely labelled nerve cells were DβH-positive (DβH+; Fig. 3b, e, h, k, n). The remaining FB+ neurons (9 ± 2.3 %) were DβH-negative (DβH-; Fig. 3b, h).Fig. 3


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 control 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 Seven fast blue-positive (FB+) neurons (a, blue, 5 long arrows, 1 short arrow, 1 double arrow), which were simultaneously DβH+ (b, green, 5 long arrows, 1 short arrow) or DβH- (1double arrow) and NPY+ (c, red, 5 long arrows, 1 double arrow) or NPY- (1 short arrow). d–f Five FB+ neurons (d, blue, 4 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 4 long arrows, 1 short arrow) and VIP+ (f, red, 4 long arrows) or VIP- (1 short arrow). g–i Four FB+ neurons (g, blue, 1 long arrow, 2 short arrows, 1 double arrow), which were simultaneously DβH+ (h, green, 1 long arrow, 2 short arrows) or DβH- (1 double arrow) and SOM+ ( i, red, 1 long arrow, 1 double arrow) or SOM- (2 short arrows). j–l Three FB+ neurons (j, blue, 3 long arrows), which were simultaneously DβH+ (k, green, 3 long arrows) and L-ENK+ (l, red, 3 long arrows). m–o Four FB+ neurons (m, blue, 1 long arrow, 3 short arrows), which were simultaneously DβH+ (n, green, 1 long arrow, 3 short arrows) and nNOS+ (o, red, 1 long arrow) or nNOS- (3 short arrows). Bars 50 μm (a–f), 20 μm (g–o)
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Fig3: Representative images of SChG-UBPN in control 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 Seven fast blue-positive (FB+) neurons (a, blue, 5 long arrows, 1 short arrow, 1 double arrow), which were simultaneously DβH+ (b, green, 5 long arrows, 1 short arrow) or DβH- (1double arrow) and NPY+ (c, red, 5 long arrows, 1 double arrow) or NPY- (1 short arrow). d–f Five FB+ neurons (d, blue, 4 long arrows, 1 short arrow), which were simultaneously DβH+ (e, green, 4 long arrows, 1 short arrow) and VIP+ (f, red, 4 long arrows) or VIP- (1 short arrow). g–i Four FB+ neurons (g, blue, 1 long arrow, 2 short arrows, 1 double arrow), which were simultaneously DβH+ (h, green, 1 long arrow, 2 short arrows) or DβH- (1 double arrow) and SOM+ ( i, red, 1 long arrow, 1 double arrow) or SOM- (2 short arrows). j–l Three FB+ neurons (j, blue, 3 long arrows), which were simultaneously DβH+ (k, green, 3 long arrows) and L-ENK+ (l, red, 3 long arrows). m–o Four FB+ neurons (m, blue, 1 long arrow, 3 short arrows), which were simultaneously DβH+ (n, green, 1 long arrow, 3 short arrows) and nNOS+ (o, red, 1 long arrow) or nNOS- (3 short arrows). Bars 50 μm (a–f), 20 μm (g–o)
Mentions: Double-labelling immunohistochemistry revealed two main populations of FB+ neurons. The vast majority (91 ± 2.3 %) of the retrogradely labelled nerve cells were DβH-positive (DβH+; Fig. 3b, e, h, k, n). The remaining FB+ neurons (9 ± 2.3 %) were DβH-negative (DβH-; Fig. 3b, h).Fig. 3

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