title: Alterations in spinal cord Fos protein expression induced by bladder stimulation following cystitis.
abstract: These studies examined Fos protein expression in spinal cord neurons synaptically activated by stimulation of bladder afferent pathways after cyclophosphamide (CYP)-induced bladder inflammation. In urethan-anesthetized Wistar rats with cystitis, intravesical saline distension significantly (P </= 0.0005) increased the number of Fos-immunoreactive (IR) cells observed in the rostral lumbar (L1, 35 cells/section; L2, 27 cells/section) and caudal lumbosacral (L6, 120 cells/section; S1, 96 cells/section) spinal cord compared with control animals, but Fos protein expression in the L5 segment was not altered. The topographical distribution of Fos-IR cells was also altered in the lumbosacral spinal cord. The majority of Fos-IR cells were distributed in the dorsal commissure (45%), with smaller percentages in the sacral parasympathetic nucleus (25%), medial dorsal horn (20%), and lateral dorsal horn (10%). These results demonstrate that urinary bladder distension produces increased numbers and an altered distribution pattern of Fos-IR cells after cystitis. This altered distribution pattern resembles that following noxious irritation of the bladder in control animals. Pretreatment with capsaicin significantly reduced the number of Fos-IR cells induced by bladder distension after cystitis. These data suggest that chronic cystitis can reveal a nociceptive Fos expression pattern in the spinal cord in response to a non-noxious bladder stimulus that is partially mediated by capasaicin-sensitive bladder afferents.
authors.affiliation: University of Vermont College of Medicine, Departments of Neurology and Anatomy and Neurobiology, Burlington, Vermont 05405, USA. mvizzard@zoo.uvm.edu
authors.forename: M A
authors.initials: MA
authors.lastname: Vizzard
mesh_terms: D019342:Acetic Acid; D018686:Anesthetics, Intravenous; D000818:Animals; D002211:Capsaicin / Q000494:pharmacology; D002795:Choline O-Acetyltransferase / Q000032:analysis; D002908:Chronic Disease; D003520:Cyclophosphamide / Q000494:pharmacology; D018856:Cystitis, Interstitial / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism*; D005260:Female; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007202:Indicators and Reagents; D008297:Male; D009412:Nerve Fibers / Q000201:enzymology / Q000276:immunology; D009619:Nociceptors / Q000187:drug effects / Q000502:physiology; D010146:Pain / Q000139:chemically induced / Q000378:metabolism; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000201:enzymology / Q000276:immunology; D010812:Physical Stimulation; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000096:biosynthesis*; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000494:pharmacology; D013116:Spinal Cord / Q000737:chemistry / Q000166:cytology / Q000378:metabolism*; D013268:Stimulation, Chemical; D007507:Therapeutic Irrigation; D014520:Urethane; D001743:Urinary Bladder / Q000294:innervation / Q000502:physiology*
chemical_list: D018686:Anesthetics, Intravenous; D007166:Immunosuppressive Agents; D007202:Indicators and Reagents; D016760:Proto-Oncogene Proteins c-fos; D014520:Urethane; D012965:Sodium Chloride; D003520:Cyclophosphamide; D002795:Choline O-Acetyltransferase; D019342:Acetic Acid; D002211:Capsaicin