Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162473 (Frey)
 2,599 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken to examine the sensory function of uterine afferent fibers in cats at unknown stages of the estrous cycle. Single unit activity was recorded from strands of the hypogastric nerve of the anesthetized cat. Once a unit was found, the conduction velocity was determined and the mechanical receptive field localized on the uterus. The response properties of the unit to mechanical stimuli applied to the receptive field and to chemical stimuli applied by intra-arterial injection of algesic chemicals (bradykinin, KCl and capsaicin) into the uterine artery were studied. Single unit activity from a total of 52 units was examined in this study. Based on the conduction velocities, about 2/3 of these fibers were found to be unmyelinated C fibers and the remaining 1/3 were thinly myelinated A delta fibers. The receptive fields of most of these fibers were located at different parts of the uterine horn and body while a few were at the uterine cervix. Mechanical thresholds, as determined by von Frey filaments applied to the external surface of the uterus, varied more than 150-fold among mechanically sensitive units, ranging from extremely low to high thresholds. In addition, most of these afferents were activated by intra-arterially injected algesic chemicals, often by more than one chemical. The data in the present study suggest that a large portion of the cat uterus is innervated by the hypogastric nerve and that these afferents originate from sensory receptors that have potentially a wide range of functions. Their potential functions as low threshold mechanoreceptors and nociceptors are discussed.
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PMID:Response properties of hypogastric afferent fibers supplying the uterus in the cat. 824 59

Interstitial cystitis (IC) is a chronic bladder inflammatory disease of unknown etiology that is often regarded as a neurogenic cystitis. IC is associated with urothelial lesions, voiding dysfunction, and pain in the pelvic/perineal area, and diet can exacerbate IC symptoms. In this study, we used a murine neurogenic cystitis model to investigate the development of pelvic pain behavior. Neurogenic cystitis was induced by the injection of Bartha's strain of pseudorabies virus (PRV) into the abductor caudalis dorsalis tail base muscle of female C57BL/6J mice. Infectious PRV virions were isolated only from the spinal cord, confirming the centrally mediated nature of this neurogenic cystitis model. Pelvic pain was assessed using von Frey filament stimulation to the pelvic region, and mice infected with PRV developed progressive pelvic pain. Pelvic pain was alleviated by 2% lidocaine instillation into either the bladder or the colon but not following lidocaine instillation into the uterus. The bladders of PRV-infected mice showed markers of inflammation and increased vascular permeability compared with controls. In contrast, colon histology was normal and vascular permeability was unchanged, suggesting that development of pelvic pain was due only to bladder inflammation. Bladder-induced pelvic pain was also exacerbated by colonic administration of a subthreshold dose of capsaicin. These data indicate organ cross talk in pelvic pain and modulation of pain responses by visceral inputs distinct from the inflamed site. Furthermore, these data suggest a mechanism by which dietary modification benefits pelvic pain symptoms.
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PMID:Organ cross talk modulates pelvic pain. 1762 30

The cause of chronic pelvic pain in interstitial cystitis/painful bladder syndrome (IC/PBS) remains unclear; autoimmunity is a possible etiology. We have recently shown that injection of a single immunogenic peptide of uroplakin 3A (UPK3A 65-84) induces experimental autoimmune cystitis (EAC) in female BALB/cJ mice that is unique among experimental models in accurately reflecting both the urinary symptoms and pelvic pain of IC/PBS. The aim of this project was to identify the roles of mast cells and mast cell chemoattractant/activator monocyte chemoattractant protein-1 [chemokine (C-C motif) ligand 2 (CCL2)] in the allodynia in this model. We immunized 6- to 8-wk-old female BALB/cJ mice with UPK3A 65-84 peptide and, 5-40 days later, observed increased responses to stimulation of the suprapubic abdominal and hindpaw surfaces with von Frey monofilaments compared with mice injected with adjuvant alone. Suprapubic and hindpaw tactile allodynia responses by EAC mice were blocked by instillation of lidocaine into the bladder but not by lidocaine in the uterus, confirming the bladder as the source of the hypersensitivity. Markedly increased numbers of activated mast cells and expression of CCL2 were found in the bladder after immunization with UPK3A 65-84. Hypersensitive responses were inhibited by mast cell stabilizer cromolyn sodium and antagonists of histamine receptors 1 and 2. Furthermore, BALB/cJ mice with deletion of the Ccl2 or chemokine (C-C motif) receptor 2 gene exhibited markedly reduced allodynia and accumulation of mast cells after UPK3A 65-84 immunization. These results show that UPK3A 65-84 immunization causes chronic visceral allodynia and suggest that it is mediated by CCL2-driven mast cell accumulation in the bladder.
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PMID:Chronic pelvic allodynia is mediated by CCL2 through mast cells in an experimental autoimmune cystitis model. 2520 62