Abstract
You have accessJournal of UrologyUrodynamics/Lower Urinary Tract Dysfunction/Female Pelvic Medicine: Neurogenic Voiding Dysfunction1 Apr 2016MP17-18 ROLE OF BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF) IN LOWER URINARY TRACT DYSFUNCTION OF MICE WITH SPINAL CORD INJURY (SCI) Naoki Wada, Takahiro Shimizu, Shun Takai, Nobutaka Shimizu, Pradeep Tyagi, William de Groat, Anthony Kanai, Hidehiro Kakizaki, and Naoki Yoshimura Naoki WadaNaoki Wada More articles by this author , Takahiro ShimizuTakahiro Shimizu More articles by this author , Shun TakaiShun Takai More articles by this author , Nobutaka ShimizuNobutaka Shimizu More articles by this author , Pradeep TyagiPradeep Tyagi More articles by this author , William de GroatWilliam de Groat More articles by this author , Anthony KanaiAnthony Kanai More articles by this author , Hidehiro KakizakiHidehiro Kakizaki More articles by this author , and Naoki YoshimuraNaoki Yoshimura More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2016.02.2686AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Brain-derived neurotrophic factor (BDNF) is reportedly involved in the plasticity of spinal neuronal pathways that induces lower urinary tract dysfunction in SCI. Although pervious BDNF studies have mainly been performed in rats, we recently reported that bladder and urethral activity is urodynamically quite different between rats and mice with SCI. Therefore, this study investigated the effects of anti-BDNF antibody treatment on storage and voiding dysfunction in mice with SCI. METHODS The Th8/9 spinal cord was transected to produce SCI in female C57BL/6N mice. Three weeks later, an osmotic pump was placed subcutaneously to administer vehicle (group A) or 10µg/kg/hr of anti-BDNF antibody (group B) for 1 week. Four weeks after transection, mice were evaluated using continuous or single-filling cystometry under a conscious condition. Then, the bladder was removed to measure BDNF levels by the ELISA method and to compare with those of spinal intact mice. RESULTS In continuous cystometry, voiding efficiency was significantly increased in the group B vs. the group A (21.4 vs. 14.1%) whereas there were no significant differences in micturition pressure (MP), intercontraction intervals or non-voiding contractions (NVC) between two groups. In single cystometry, voided volume (0.085 vs. 0.038 ml) and voiding efficiency (42.3 vs. 18.4%) in the group B were significantly increased compared to the group A. MP, maximum cystometric capacity or NVC was not different between two groups. The BDNF level of the group A bladder was significantly higher than that of normal mice (5.29±0.45 vs. 1.38±0.18 pg/mg tissue); however, it was decreased in the group B bladder (1.69±0.26 pg/mg tissue) compared to the group A. CONCLUSIONS The anti-BDNF antibody treatment, which reduced bladder BDNF expression, improved voiding dysfunction as shown by increases in voided volume and voiding efficiency, but did not affect storage dysfunction as evidenced by unaltered NVCs in SCI mice. These results suggest that increased BDNF after SCI contributes to inefficient voiding, possibly due to impaired coordinating activity of bladder and urethra during voiding. Thus, BDNF-targeting therapies could be effective for treating voiding problems in SCI patients. © 2016FiguresReferencesRelatedDetails Volume 195Issue 4SApril 2016Page: e191 Advertisement Copyright & Permissions© 2016MetricsAuthor Information Naoki Wada More articles by this author Takahiro Shimizu More articles by this author Shun Takai More articles by this author Nobutaka Shimizu More articles by this author Pradeep Tyagi More articles by this author William de Groat More articles by this author Anthony Kanai More articles by this author Hidehiro Kakizaki More articles by this author Naoki Yoshimura More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
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