Botulinum Toxin Type A Induces Changes in the Chemical Coding of Substance P-Immunoreactive Dorsal Root Ganglia Sensory Neurons Supplying the Porcine Urinary Bladder

• Main Authors: Agnieszka Bossowska, Ewa Lepiarczyk, Urszula Mazur, Paweł Janikiewicz, Włodzimierz Markiewicz
• Format: Article
• Language: English
• Published: MDPI AG 2015-11-01
• Series: Toxins
• Subjects: botulinum toxin A; urinary bladder; sensory innervation; dorsal root ganglia; substance P; neurotransmitters; pain; immunohistochemistry; pig
• Online Access: http://www.mdpi.com/2072-6651/7/11/4797

Botulinum toxin (BTX) is a potent neurotoxin which blocks acetylcholine release from nerve terminals, and therefore leads to cessation of somatic motor and/or parasympathetic transmission. Recently it has been found that BTX also interferes with sensory transmission, thus, the present study was aimed at investigating the neurochemical characterization of substance P-immunoreactive (SP-IR) bladder-projecting sensory neurons (BPSN) after the toxin treatment. Investigated neurons were visualized with retrograde tracing method and their chemical profile was disclosed with double-labelling immunohistochemistry using antibodies against SP, calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase activating polypeptide (PACAP), neuronal nitric oxide synthase (nNOS), galanin (GAL), calbindin (CB), and somatostatin (SOM). In the control group (n = 6), 45% of the total population of BPSN were SP-IR. Nearly half of these neurons co-expressed PACAP or CGRP (45% and 35%, respectively), while co-localization of SP with GAL, nNOS, SOM or CB was found less frequently (3.7%, 1.8%, 1.2%, and 0.7%, respectively). In BTX-treated pigs (n = 6), toxin-injections caused a decrease in the number of SP-IR cells containing CGRP, SOM or CB (16.2%, 0.5%, and 0%, respectively) and a distinct increase in these nerve cells immunopositive to GAL (27.2%). The present study demonstrates that BTX significantly modifies the chemical phenotypes of SP-IR BPSN.