{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T22:00:05Z","timestamp":1774735205018,"version":"3.50.1"},"reference-count":24,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,9,27]],"date-time":"2016-09-27T00:00:00Z","timestamp":1474934400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurourology and Urodynamics"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:sec><jats:title>Aims<\/jats:title><jats:p>There are some reports that bladder C\u2010fibers are partially involved in detrusor overactivity in patients with brain lesions. We investigated the contribution of bladder C\u2010fiber to decreased bladder capacity in rats with cerebral infarction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Cerebral infarction was induced under halothane anesthesia by left middle cerebral artery occlusion with 4\u20100 nylon thread in female Sprague\u2010Dawley rats. Intramural amounts of\u2009ATP and prostaglandin E<jats:sub>2<\/jats:sub>, in vivo and in vitro ATP, NGF, and prostaglandin E<jats:sub>2<\/jats:sub> release from the distended bladder urothelium, and changes in mRNA expressions of sensor molecules and receptors were monitored 6\u2009h after the occlusion. Cystometry was performed in rats with or without resiniferatoxin pretreatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Overexpression of sensor molecule, transient receptor potential vanilloid\u2010type channel 1, acid\u2010sensing ion channel 2, purinergic receptors P2X<jats:sub>3<\/jats:sub>, and M<jats:sub>2<\/jats:sub>\/M<jats:sub>3<\/jats:sub> muscarinic receptors was found in the bladder. These changes were accompanied by increases in ATP and NGF release from the urothelium. In contrast, when bladder C\u2010fibers were desensitized by resiniferatoxin, no increase in NGF release from the urothelium was found either in vivo or in vitro. There was no difference in the percentage decrease in bladder capacity between cerebral infarction rats pretreated with resiniferatoxin and cerebral infarction rats without pretreatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Results indicate that expression of sensor molecules in the bladder is altered by distant infarction in the brain. ATP and NGF release from the urothelium also increased. NGF release was related to activation of bladder C\u2010fibers. Bladder C\u2010fibers might not contribute much to decreased bladder capacity caused by cerebral infarction.<\/jats:p><\/jats:sec>","DOI":"10.1002\/nau.23142","type":"journal-article","created":{"date-parts":[[2016,9,27]],"date-time":"2016-09-27T12:43:44Z","timestamp":1474980224000},"page":"1448-1455","source":"Crossref","is-referenced-by-count":9,"title":["Nerve growth factor release from the urothelium increases via activation of bladder C\u2010fiber in rats with cerebral infarction"],"prefix":"10.1002","volume":"36","author":[{"given":"Ryusei","family":"Yokokawa","sequence":"first","affiliation":[{"name":"Faculty of Medical Science, Department of Urology University of Fukui Fukui Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hironobu","family":"Akino","sequence":"additional","affiliation":[{"name":"Faculty of Medical Science, Department of Urology University of Fukui Fukui 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