Expression of neuropeptides and nitric oxide synthase in neurones innervating the inflamed rat urinary bladder

Callsen-Cencic, Peter; Mense, Siegfried

doi:10.1016/s0165-1838(97)00032-5

Cited by 66 publications

(58 citation statements)

References 54 publications

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“…Neurogenic components of this inflammation include the release of proinflammatory neurotransmitters by the peripheral branch of sensory and autonomic postganglionic neurons, together with activation of C NS bladder circuits Lantéri-Minet et al, 1995;Bon et al, 1996;Vizzard et al, 1996;C allsen-C encic and Mense, 1997). It remains unknown whether these C NS circuits are conscripted as epipathogenic co-factors to an essentially peripheral phenomenon.…”

Section: Abstract: Neuroimmune Process; Herpesviridae Infection; Nitmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

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Section: Abstract: Neuroimmune Process; Herpesviridae Infection; Nitmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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“…CGRP acts synergistically with SP in the spinal cord (Biella et al 1991) and such synergism may result from CGRP-mediated inhibition of an endopeptidase that degrades SP (Le Greves et al 1985), thus elevating the local concentration of SP at the site of release. It has been shown that cystitis leads to a significant rise in the number of CGRP-IR bladder-projecting cells in rats (Callsen-Cencic andMense 1997, Vizzard 2001). This may be suggestive for an involvement of CGRP in the sensitization of afferent neuronal pathways in the lower urinary tract and for a role of CGRP in mediation of bladder overactivity (Vizzard 2001).…”

Section: Discussionmentioning

confidence: 99%

“…One of the crucial elements of reflex arc, participating in the regulation of the urinary bladder physiological functions, are DRGs sensory neurons. It has been shown in the past that in different species, including the rat, guinea pig, cat and pig (Habler et al 1990, Callsen-Cencic and Mense 1997, Zhou and Ling 1997, Bossowska et al 2009), the urinary bladder receives afferent innervation from sensory neurons located in thoraco-lumbar (rat and cat), lumbar (guinea pig and pig), lumbar-sacral (rat and guinea pig), sacral (cat) or sacro-coccygeal DRGs (pig) ganglia. Thus, urinary bladder-projecting sensory neurons occurring in two different locations, probably transmit stimuli that leads to a regulation of the urinary bladder activity.…”

Section: Introductionmentioning

confidence: 99%

“…It has also been suggested that detrusor hyperexcitability is mainly due to alterations in the afferent innervation of the bladder, mainly connected with changes in neurotransmitters expression in bladder sensory neurons. For example, it has been shown in rats that the induction of cystitis leads to a significant increase in the number of SP-, CGRP-, PACAP-, GAL-and NOS-immunoreactive (IR) bladder afferent nerve cells (Callsen-Cencic and Mense 1997, Vizzard 2000, 2001. Thus, taking into consideration that the hyperactivity or an abnormal activity of separate elements of the nervous system participating in the regulation of the lower urinary tract functions may be the main reason of numerous urinary bladder disorders, several neurotoxins have been introduced in experimental therapies of such illnesses.…”

Section: Introductionmentioning

confidence: 99%

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The influence of resiniferatoxin on the chemical coding of neurons in dorsal root ganglia supplying the urinary bladder in the female pig

Bossowska¹,

Majewski²

2012

Polish Journal of Veterinary Sciences

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Although resiniferatoxin (RTX) becomes more often used in experimental therapies of sensory system disorders, so far there is no data concerning the influence of RTX on the chemical coding of neurons in dorsal root ganglia (DRG) supplying the urinary bladder in the pig, an animal species considered as a reliable animal model for investigation dealing with human lower urinary tract disorders. Retrograde tracer Fast Blue (FB) was injected into the wall of the right half of the urinary bladder in six juvenile female pigs, and three weeks later, bladder instillation of RTX (500 nmol per animal) was carried out in all the animals. After a week, DRGs were harvested from all the pigs and the neurochemical characterization of FB + neurons was performed using routine single-immunofluorescence labeling technique on 10-μm-thick cryostat sections. RTX instillation resulted in a distinct decrease in the numbers of FB + cells containing calcitonin gene-related peptide (CGRP), nitric oxide synthase (NOS), somatostatin (SOM) and calbindin (CB) when compared with those found in the healthy animals (18% vs. 36%, 1% vs. 6%, 0.8% vs. 4% and 0.5% vs. 3%, respectively), and an increase in the number of pituitary adenylate cyclase-activating polypeptide (PACAP)-and galanin (GAL)-immunoreactive (IR) nerve cells (51% vs. 26% and 47% vs. 6.5%). The results obtained suggest that RTX could be taken into consideration when the neuroactive agents are planned to be used in experimental therapies of selected neurogenic bladder illnesses.

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“…Animal studies show that when the infection is intense enough to cause rupture of the endothelium, there is an afferent stimulus in response to vesical distension (13), with the prompt onset of rhythmic vesical contractions (14). Immunohistochemical studies of the inflammated bladder showed a an increased expression of nociceptive neuropeptides such as substance P and calcitonine generelated peptides, described in women with vesical instability (15).…”

Section: Discussionmentioning

confidence: 99%

Etiology of urinary tract infection in scholar children

Barroso¹,

Barroso²,

Jacobino³

et al. 2003

Int. braz j urol.

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Objective: To prospectively assess the prevalence of vesicourethral dysfunction in children over 3 years old, comparing it with the occurrence rate for other potential factors that cause urinary infection in this age range.Materials and Methods: 36 girls and 9 boys were assessed, with mean age of 6.4 years, ranging from 3 to 13.9 years. These children were prospectively assessed regarding the presence of symptoms of lower urinary tract dysfunction. These data were compared with the retrospective assessment of other potential risk factors for urinary infection. Ultrasonography was performed in 28 children and voiding cystourethrogram was performed in 26 patients.Results: Vesicourethral dysfunction was diagnosed in 39 (87%) of the 45 children with urinary infection. Among these 39 patients, all had voiding urgency, 30 (77%) had urinary incontinence, 12 (31%) pollakiuria and 3 (8%) presented infrequent voiding. Vaginal discharge was evidenced in 8 (22%) girls and phimosis in 2 (22%) boys. Obstipation was diagnosed in 10 (22%) cases. Significant post-voiding residue was detected in 4 (13%) of the 28 cases assessed. Vesicoureteral reflux was evidenced in 5 (19%) of the 26 patients who underwent voiding cystourethrogram. In only 2 (4%) cases there was not an apparent cause for the infection.Conclusion: Vesicourethral dysfunction is a major cause of urinary infection in children with ages above 3 years old. In cases where voiding dysfunction in not present, other predisposing factors must be assessed. However, only 4% of the patients did not present an apparent urologic cause for the infection.

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Expression of neuropeptides and nitric oxide synthase in neurones innervating the inflamed rat urinary bladder

Cited by 66 publications

References 54 publications

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

The influence of resiniferatoxin on the chemical coding of neurons in dorsal root ganglia supplying the urinary bladder in the female pig

Etiology of urinary tract infection in scholar children

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