Abstract

You have accessJournal of UrologyCME1 May 2022MP07-20 CENTRALLY ADMINISTERED CORTICOTROPIN-RELEASING FACTOR INDUCES FACILITATION OF THE RAT MICTURITION VIA BRAIN GLUTAMATERGIC RECEPTORS Takahiro Shimizu, Yurika Hata, Suo Zou, Masaki Yamamoto, Hideaki Ono, Yohei Shimizu, Takaaki Aratake, Shogo Shimizu, Youichirou Higashi, Takashi Karashima, and Motoaki Saito Takahiro ShimizuTakahiro Shimizu More articles by this author , Yurika HataYurika Hata More articles by this author , Suo ZouSuo Zou More articles by this author , Masaki YamamotoMasaki Yamamoto More articles by this author , Hideaki OnoHideaki Ono More articles by this author , Yohei ShimizuYohei Shimizu More articles by this author , Takaaki AratakeTakaaki Aratake More articles by this author , Shogo ShimizuShogo Shimizu More articles by this author , Youichirou HigashiYouichirou Higashi More articles by this author , Takashi KarashimaTakashi Karashima More articles by this author , and Motoaki SaitoMotoaki Saito More articles by this author View All Author Informationhttps://doi.org/10.1097/JU.0000000000002529.20AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract INTRODUCTION AND OBJECTIVE: Roles of brain corticotropin-releasing factor (CRF), a representative stress-related neuropeptide, in regulation of the micturition are still controversial. In this study, we examined the effects of centrally administered CRF on the rat micturition and central mechanisms for the CRF-induced responses, focusing on brain CRF1/CRF2 receptor subtypes and glutamatergic receptors (NMDA and AMPA subtypes). METHODS: In urethane anesthetized (0.8 g/kg, ip) male Wistar rats (300-450 g), a catheter was inserted into the bladder to perform cystometry (CMG, 12 ml/h saline infusion). CRF (1 or 3 nmol/rat) or vehicle was intracerebroventricularly (icv) administered 3 h after the surgery. In some rats, effects of icv pretreated CP154526 (CP, CRF1 antagonist, 30 or 100 nmol/rat), K41498 (K, CRF2 antagonist, 30 nmol/rat), MK-801 (MK, NMDA receptor antagonist, 3 or 10 nmol/rat) or DNQX (AMPA receptor antagonist, 1 or 3 nmol/rat) on the CRF (3 nmol/rat, icv)-induced responses were examined. Continuous CMG and evaluation of intercontraction intervals (ICI) and maximal voiding pressure (MVP) were started 1 h before the first icv administration. When performing single CMG 3 h after the surgery, after 4-5 times of single CMG, CRF (3 nmol/rat) or vehicle was icv administered, then single CMG was performed during 60-120 min after the administration. RESULTS: CRF dose-dependently shortened ICI (Fig. 1A) without changing MVP (data not shown). The CRF-induced ICI shortening was suppressed by CP, MK-801 and DNQX (Fig. 1B and Fig. 2), but not by K (data not shown). Compared to the vehicle-treated group, CRF significantly reduced single-voided volume and bladder capacity without changing post void residual volume or voiding efficiency (Table 1). CONCLUSIONS: Centrally administered CRF induces facilitation of the rat micturition via brain CRF1, NMDA and AMPA receptors, therefore, brain CRF1 receptors might be new therapeutic targets for neurogenic bladder overactivity. Source of Funding: JSPS KAKENHI (#20K07827), Takeda Science Foundation © 2022 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 207Issue Supplement 5May 2022Page: e123 Advertisement Copyright & Permissions© 2022 by American Urological Association Education and Research, Inc.MetricsAuthor Information Takahiro Shimizu More articles by this author Yurika Hata More articles by this author Suo Zou More articles by this author Masaki Yamamoto More articles by this author Hideaki Ono More articles by this author Yohei Shimizu More articles by this author Takaaki Aratake More articles by this author Shogo Shimizu More articles by this author Youichirou Higashi More articles by this author Takashi Karashima More articles by this author Motoaki Saito More articles by this author Expand All Advertisement PDF DownloadLoading ...

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