Abstract
Although guanethidine (GUA) was used in the past as a drug to suppress hyperactivity of the sympathetic nerve fibers, there are no available data concerning the possible action of this substance on the sensory component of the peripheral nervous system supplying the urinary bladder. Thus, the present study was aimed at disclosing the influence of intravesically instilled GUA on the distribution, relative frequency, and chemical coding of dorsal root ganglion neurons associated with the porcine urinary bladder. The investigated sensory neurons were visualized with a retrograde tracing method using Fast Blue (FB), while their chemical profile was disclosed with single-labeling immunohistochemistry using antibodies against substance P (SP), calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase activating polypeptide (PACAP), galanin (GAL), neuronal nitric oxide synthase (nNOS), somatostatin (SOM), and calbindin (CB). After GUA treatment, a slight decrease in the number of FB+ neurons containing SP was observed when compared with untreated animals (34.6 ± 6.5% vs. 45.6 ± 1.3%), while the number of retrogradely traced cells immunolabeled for GAL, nNOS, and CB distinctly increased (12.3 ± 1.0% vs. 7.4 ± 0.6%, 11.9 ± 0.6% vs. 5.4 ± 0.5% and 8.6 ± 0.5% vs. 2.7 ± 0.4%, respectively). However, administration of GUA did not change the number of FB+ neurons containing CGRP, PACAP, or SOM. The present study provides evidence that GUA significantly modifies the sensory innervation of the porcine urinary bladder wall and thus may be considered a potential tool for studying the plasticity of this subdivision of the bladder innervation.
Highlights
It should be stressed that, in both earlier studies, the control groups were slightly different: while in the case of the study focusing on neurochemical characterization of UBPNs [6], no medical procedures were applied to the control animals, in the present study, as well as in an earlier work concerning the influence of botulinum toxin type A (BTX) on the plasticity of substance P (SP)+ bladderprojecting dorsal root ganglion (DRG) neurons, the control animals were intravesically instilled either with citrate buffer or with 5% aqueous solution of ethyl alcohol (BTX study) [28]
The present study has shown that GUA instillation induced a down-regulation in the number of SP-IR and, concomitantly, an up-regulation in numbers of GAL, neuronal nitric oxide synthase (nNOS), or CB-containing urinary bladder afferent neurons, while the numbers of calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase activating polypeptide (PACAP), or SOM-containing bladder-projecting sensory cells remained unchanged
Results of the present study clearly demonstrated that GUA, instilled into the porcine urinary bladder, was able to evoke a distinct increase in the number of GAL, nNOS, and CB-IR sensory neurons supplying this organ
Summary
The storage and periodic elimination of urine requires a complex neural control system that coordinates the activity of a variety of effector organs, including smooth muscles of the urinary bladder [1]. One of the crucial elements of such reflex arc, participating in the regulation of the urinary bladder physiological functions, is dorsal root ganglion (DRG). Spinal afferent neurons are responsible for transmission of sensations from the bladder, which range from fullness and urgency to discomfort and pain. Working together with sympathetic and parasympathetic efferent nerves, spinal afferent neurons play a key role in reflex control of urinary storage and micturition. Sensory innervation of the urinary bladder has been found to originate in humans, rats, guinea pigs, and cats [2,3,4,5]
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