Up‐regulation of pituitary adenylate cyclase‐activating polypeptide in urinary bladder pathways after chronic cystitis

Vizzard, Margaret A.

doi:10.1002/(sici)1096-9861(20000508)420:3<335::aid-cne5>3.0.co;2-#

Cited by 93 publications

(103 citation statements)

References 56 publications

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“…Although no neurons are selectively activated by distension of the colon, the majority of bladderresponsive neurons (73%) are also activated by colon distension. These data support the proposals based on PRV tracing experiments that neurons in the PMC coordinate the functions of the colon and the LUT (526, 655, 659). Retrograde axonal tracing experiments in rats in which different color fluorescent beads were injected into the sacral parasympathetic nucleus of the S1–S2 segments (red) and into the thoraco-lumbar sympathetic nucleus at T13-L1 segments (green) revealed two populations spinal projecting neurons in the PMC: preparasympathetic output (PPO) and presympathetic output (PSO) neurons (250).…”

Section: Voiding Mechanismssupporting

confidence: 89%

“…Dual PRV tracing in which different tracers were injected into the colon and bladder revealed that three populations of neurons are present in Barrington’s nucleus: (i) bladder labeled, (ii) colon labeled, and (iii) neurons synaptically linked to both organs (526). These experiments suggest that neurons in this nucleus are involved in the control of multiple excretory functions (527, 655, 659). …”

Section: Anatomy Of the Spinal Pathways Controlling The Lower Urinarymentioning

confidence: 86%

“…Immunohistochemical studies reveal that bladder afferent neurons contain various neuropeptides such as substance P (SP), calcitonin gene-related peptide (CGRP), pituitary adenylate cyclase-activating polypeptide (PACAP), and VIP (162,321, 394, 659, 660) as well as putative excitatory amino acid transmitters, glutamic and aspartic acid (323), and vesicular glutamate transporters (82). Peptide-containing axons are distributed throughout all layers of the bladder but are particularly dense in the lamina propria just beneath the urothelium.…”

Section: Peripheral Nervous Systemmentioning

confidence: 99%

“…Neurons in Barrington’s nucleus in the rat are also labeled after injections of PRV into the colon (497, 655, 659). Dual PRV tracing in which different tracers were injected into the colon and bladder revealed that three populations of neurons are present in Barrington’s nucleus: (i) bladder labeled, (ii) colon labeled, and (iii) neurons synaptically linked to both organs (526).…”

Section: Anatomy Of the Spinal Pathways Controlling The Lower Urinarymentioning

confidence: 99%

“…Chemical inflammation of the rat urinary bladder also induces increased expression of various chemical markers in afferent neurons in lumbosacral DRG innervating the bladder (33), such as NOS (663), growth-associated protein (GAP-43) (662), PACAP (659), neuropeptides such as substance P (660), PARs (140), cyclooxygenase-2 (COX-2), and prostaglandins (276). Some of these changes may also contribute to the development of afferent sensitization.…”

Section: Disease-induced Changes In Micturitionmentioning

confidence: 99%

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Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

348

527

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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Section: Voiding Mechanismssupporting

confidence: 89%

Section: Anatomy Of the Spinal Pathways Controlling The Lower Urinarymentioning

confidence: 86%

Section: Peripheral Nervous Systemmentioning

confidence: 99%

Section: Anatomy Of the Spinal Pathways Controlling The Lower Urinarymentioning

confidence: 99%

Section: Disease-induced Changes In Micturitionmentioning

confidence: 99%

See 3 more Smart Citations

Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

348

527

View full text Add to dashboard Cite

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Up‐regulation of tyrosine kinase (Trka, Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord (T8–T10) injury

Qiao

Vizzard

2002

J of Comparative Neurology

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Previous studies have demonstrated changes in urinary bladder neurotrophic factors after bladder dysfunction. We have hypothesized that retrograde transport of neurotrophin(s) from the bladder to lumbosacral dorsal root ganglia (DRG) may play a role in bladder reflex reorganization after spinal cord injury (SCI). In this study, we determined whether the expression of tyrosine kinase receptors (TrkA, TrkB) is altered in lumbosacral DRG after SCI through immunofluorescence techniques. Complete transection of the spinal cord (T8-T10) was performed in female Wistar rats (120-150 g), and animals were studied 5-6 weeks after SCI. One week before killing, Fast Blue (FB) was injected into the bladder to label bladder afferent cells in the L1, L2, L6, and S1 DRG. After SCI, a significant increase in the number of TrkA-immunoreactive (IR) positive cells was detected in the L6-S1 DRG (L6: 1.9-fold, P < or = 0.01; S1: 1.7-fold, P < or = 0.05) and in the L1 DRG (3.0-fold; P < or = 0.01) but not in the L4-L5 DRG compared with spinal-intact (control) rats. After SCI, a significant increase in the number of TrkB-IR cells was also detected in the L6-S1 DRG (L6: 2.2-fold, P < or = 0.01; S1: 1.5-fold, P < or = 0.05) and in the L1-L2 DRG (L1: 1.5-fold, P < or = 0.01; L2: 1.3-fold, P < or = 0.05) but not in the L4-L5 DRG compared with control rats. After SCI, the percentage of FB-labeled cells expressing TrkA immunoreactivity (approximately 68%) or TrkB immunoreactivity (approximately 65%) in L1 and L6 DRG significantly (P < or = 0.01) increased compared with control (20-30%) DRG. After SCI, the percentage of TrkA-IR cells expressing phosphorylated (p)-Trk immunoreactivity significantly increased (1.5- to 2.3-fold increase) in the L1, L6, and S1 DRG. The percentage of TrkB-IR cells expressing p-Trk immunoreactivity after SCI also increased (1.3-fold increase) in the L1 and L6 DRG. These results demonstrate that (1) TrkA and TrkB immunoreactivity is increased in bladder afferent cells after SCI and (2) TrkA and TrkB receptors are phosphorylated in DRG after SCI. Neuroplasticity of lower urinary tract reflexes after SCI may be mediated by both nerve growth factor and brain-derived neurotrophic factor.

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Cystitis‐induced upregulation of tyrosine kinase (TrkA, TrkB) receptor expression and phosphorylation in rat micturition pathways

Qiao

Vizzard

2002

J of Comparative Neurology

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This study examined tyrosine kinase receptor (Trk) expression and phosphorylation in lumbosacral dorsal root ganglia (DRG) after acute (8 or 48 hours) or chronic (10 days) cyclophosphamide (CYP)-induced cystitis. Increases in the number of TrkA-immunoreactive (IR) cell profiles were detected in the L1 and L6 DRG (four-fold; P < or = 0.01) and the S1 DRG (1.5-fold; P < or = 0.05) but not in the L2, L4, and L5 DRG with CYP-induced cystitis of acute and chronic duration compared with control rats. The number of TrkB-IR cell profiles increased in the L1 and L2 DRG (L1: 2.6-fold; L2: 1.4-fold; P < or = 0.05) and in the L6 and S1 DRG (L6: 2.2-fold; S1: 1.3-fold; P < or = 0.05) only after acute CYP treatment (8 hours). After CYP treatment, the percentage of bladder afferent cell profiles expressing TrkA-IR (approximately 50%; P < or = 0.05) increased in L1 and L6 DRG. The percentage of bladder afferent cell profiles expressing TrkB-IR (approximately 45%; P < or = 0.05) in L1, L2, L6, and S1 DRG also increased compared with control cell profiles. The increase in TrkA-IR in bladder afferent cells occurred 8 hours after CYP treatment and was maintained in L1 DRG with chronic (10 days) CYP-induced cystitis. However, the increase in bladder afferent cells expressing TrkB-IR only occurred at the most acute time point examined (8 hours). TrkA-IR and TrkB-IR cell profiles also demonstrated phosphorylated Trk-IR with acute and/or chronic CYP-induced cystitis. These results demonstrated that CYP-induced cystitis increases the expression and phosphorylation of Trk receptors in lumbosacral DRG. Expression of neurotrophic factors in the inflamed urinary bladder may contribute to this increased expression, and neurotrophic factor and Trk interactions may play unique roles in decreased urinary tract plasticity with CYP-induced cystitis.

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Up‐regulation of pituitary adenylate cyclase‐activating polypeptide in urinary bladder pathways after chronic cystitis

Cited by 93 publications

References 56 publications

Neural Control of the Lower Urinary Tract

Neural Control of the Lower Urinary Tract

Up‐regulation of tyrosine kinase (Trka, Trkb) receptor expression and phosphorylation in lumbosacral dorsal root ganglia after chronic spinal cord (T8–T10) injury

Cystitis‐induced upregulation of tyrosine kinase (TrkA, TrkB) receptor expression and phosphorylation in rat micturition pathways

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